Bio

Academic Appointments


Administrative Appointments


  • Managing Scientist (Consultant), Exponent, Inc., Health Sciences Practice (2012 - Present)
  • Research Scientist, Cancer Prevention Institute of California (formerly the Northern California Cancer Center) (2005 - 2012)
  • Chief Epidemiologist, Asian Liver Center at Stanford University (2006 - 2011)

Professional Education


  • Post-doc, Karolinska Institute, Medical Epidemiology & Biostatistics (2005)
  • Sc.D., Harvard School of Public Health, Epidemiology (2003)
  • A.B., Harvard College, English & American Lit. & Lang. (1998)

Research & Scholarship

Current Research and Scholarly Interests


• Hodgkin lymphoma: Dr. Chang and colleagues found that variation in inflammatory genes may also be associated with risk of Hodgkin lymphoma risk, and she is currently pursuing other studies of genetic susceptibility and gene-environment interactions in Hodgkin lymphoma development. Previously, in a population-based case-control study led by Dr. Nancy Mueller of the Harvard School of Public Health, Dr. Chang investigated how determinants of childhood social environment and infection were associated with Hodgkin lymphoma risk, and how serum levels of antibodies against the Epstein-Barr virus (EBV)and other risk factors varied between EBV-positive and EBV-negative Hodgkin lymphoma. Also, using data from Swedish population registries, Dr. Chang studied the association of sibship size with Hodgkin lymphoma risk, and examined seasonal patterns in the incidence of Hodgkin lymphoma among children and young adults.

• Non-Hodgkin lymphoma: Much of Dr. Chang’s research has aimed to clarify the roles of immune function, genetic susceptibility, and environmental exposures in the development of non-Hodgkin lymphomas. She led a study of vitamin D, ultraviolet radiation, and risk of lymphoid malignancies in the California Teachers Study, a prospective cohort study of over 130,000 female California public school teachers and administrators. Much of Dr. Chang’s previous research was based within a population-based case-control study of malignant lymphoma in Denmark and Sweden, led by Prof. Mads Melbye of the Statens Serum Institute and Prof. Hans-Olov Adami of the Karolinska Institute. Dr. Chang's research in this study included investigations of the roles of viral and bacterial infections, diet and alcohol, tobacco smoking, childhood social environment, body mass index, medication use, family history of hematopoietic malignancy, prior autoimmune disease, and genetic susceptibility in the development of non-Hodgkin and Hodgkin lymphomas.

• Hepatocellular carcinoma: Dr. Chang worked with Drs. Samuel So, Mei-Sze Chua, and colleagues at the Asian Liver Center at Stanford to investigate the etiology and prevention of hepatocellular carcinoma. Part of their research involved translating genomic and proteomic data into useful clinical biomarkers for hepatocellular carcinoma. In addition, Dr. Chang played an active role in the Asian Liver Center’s community-based outreach and education programs aiming to prevent hepatitis B and liver cancer in Asians and Pacific Islanders. Dr. Chang also partnered with Dr. Mindie Nguyen of the Stanford Hepatology Clinic and colleagues at the Stanford Human Immune Monitoring Center to investigate the role of cytokines in chronic hepatitis and hepatocellular carcinoma.

• Nasopharyngeal carcinoma: Dr. Chang is part of an international team of collaborators (in China, the U.S., and Sweden) conducting a large, population-based case-control study of nasopharyngeal carcinoma in Southeast China, where this malignancy is endemic. The study aims to elucidate the interactions of genetic susceptibility, environmental exposures, and viral infection (with EBV) in the development of nasopharyngeal carcinoma.

• Lung cancer in non-smokers: Dr. Chang collaborated with Drs. Scarlett Lin Gomez and Heather Wakelee of the Stanford Cancer Center on several studies of lung cancer in non-smokers. Dr. Chang led a pilot study to identify motivations and deterrents for participation in health research studies among Asian/Pacific Islander and Latina women, with the goal of eventually developing a population-based case-control study of non-smoking-associated lung cancer in these population groups with a low prevalence of smoking. In addition, Drs. Chang, Gomez, and Wakelee have collaborated on studies of lung cancer survival in non-smokers and in Asians/Pacific Islanders.

Teaching

Graduate and Fellowship Programs


Publications

Journal Articles


  • Exposure to UV radiation and risk of Hodgkin lymphoma: a pooled analysis. Blood Monnereau, A., Glaser, S. L., Schupp, C. W., Ekström Smedby, K., de Sanjosé, S., Kane, E., Melbye, M., Forétova, L., Maynadié, M., Staines, A., Becker, N., Nieters, A., Brennan, P., Boffetta, P., Cocco, P., Glimelius, I., Clavel, J., Hjalgrim, H., Chang, E. T. 2013; 122 (20): 3492-3499

    Abstract

    Ultraviolet radiation (UVR) exposure has been inversely associated with Hodgkin lymphoma (HL) risk, but only inconsistently, only in a few studies, and without attention to HL heterogeneity. We conducted a pooled analysis of HL risk focusing on type and timing of UVR exposure and on disease subtypes by age, histology, and tumor-cell Epstein-Barr virus (EBV) status. Four case-control studies contributed 1320 HL cases and 6381 controls. We estimated lifetime, adulthood, and childhood UVR exposure and history of sunburn and sunlamp use. We used 2-stage estimation with mixed-effects models and weighted pooled effect estimates by inverse marginal variances. We observed statistically significant inverse associations with HL risk for UVR exposures during childhood and adulthood, sunburn history, and sunlamp use, but we found no significant dose-response relationships. Risks were significant only for EBV-positive HL (pooled odds ratio, 0.56; 95% confidence interval, 0.35 to 0.91 for the highest overall UVR exposure category), with a significant linear trend for overall exposure (P = .03). Pooled relative risk estimates were not heterogeneous across studies. Increased UVR exposure may protect against HL, particularly EBV-positive HL. Plausible mechanisms involving UVR induction of regulatory T cells or the cellular DNA damage response suggest opportunities for new prevention targets.

    View details for DOI 10.1182/blood-2013-04-497586

    View details for PubMedID 24016459

  • Risk of lymphoma subtypes after solid organ transplantation in the United States BRITISH JOURNAL OF CANCER Clarke, C. A., Morton, L. M., Lynch, C., Pfeiffer, R. M., Hall, E. C., Gibson, T. M., Weisenburger, D. D., Martinez-Maza, O., Hussain, S. K., Yang, J., Chang, E. T., Engels, E. A. 2013; 109 (1): 280-288

    Abstract

    Background:Solid organ transplant recipients have high risk of lymphomas, including non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL). A gap in our understanding of post-transplant lymphomas involves the spectrum and associated risks of their many histologic subtypes.Methods:We linked nationwide data on solid organ transplants from the US Scientific Registry of Transplant Recipients (1987-2008) to 14 state and regional cancer registries, yielding 791 281 person-years of follow-up for 19 distinct NHL subtypes and HL. We calculated standardised incidence ratios (SIRs) and used Poisson regression to compare SIRs by recipient age, transplanted organ, and time since transplantation.Results:The risk varied widely across subtypes, with strong elevations (SIRs 10-100) for hepatosplenic T-cell lymphoma, Burkitt's lymphoma, NK/T-cell lymphoma, diffuse large B-cell lymphoma, and anaplastic large-cell lymphoma (both systemic and primary cutaneous forms). Moderate elevations (SIRs 2-4) were observed for HL and lymphoplasmacytic, peripheral T-cell, and marginal zone lymphomas, but SIRs for indolent lymphoma subtypes were not elevated. Generally, SIRs were highest for younger recipients (<20 years) and those receiving organs other than kidneys.Conclusion:Transplant recipients experience markedly elevated risk of a distinct spectrum of lymphoma subtypes. These findings support the aetiologic relevance of immunosuppression for certain subtypes and underscore the importance of detailed haematopathologic workup for transplant recipients with suspected lymphoma.British Journal of Cancer advance online publication, 11 June 2013; doi:10.1038/bjc.2013.294 www.bjcancer.com.

    View details for DOI 10.1038/bjc.2013.294

    View details for Web of Science ID 000321702400036

    View details for PubMedID 23756857

  • Body size and risk of Hodgkin's lymphoma by age and gender: a population-based case-control study in Connecticut and Massachusetts CANCER CAUSES & CONTROL Li, Q., Chang, E. T., Bassig, B. A., Dai, M., Qin, Q., Gao, Y., Zhang, Y., Zheng, T. 2013; 24 (2): 287-295

    Abstract

    Descriptive studies have indicated a rising trend in Hodgkin's lymphoma (HL) incidence in young adults, especially females. Increasing evidence has suggested that some risk factors associated with HL may vary by age or gender. Recent studies have reported an increased risk of HL associated with increasing body mass index (BMI), but the results have been inconsistent. The objectives of this study were to examine whether the associations between measures of body size (height, weight, and BMI) and HL risk vary by age and/or gender.A population-based case-control study was conducted in Connecticut and Massachusetts. A total of 567 HL cases and 679 controls were recruited in 1997-2000. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95 % confidence intervals (CIs).Among younger women <35 years old, being overweight (25-29.9 kg/m(2)) versus normal weight (18.5-24.9 kg/m(2)) was significantly associated with an increased risk of HL (OR = 2.1, 95 % CI = 1.1-4.0). The risk increased with increasing weight and BMI (p trends <0.01). Among women ?35 years old, by contrast, higher weight and BMI were associated with a reduced risk of HL (p trends <0.01). Conversely, there was no significant association between BMI and risk of HL in younger or older males.These findings show that the associations between body size and risk of HL vary by gender and age, and require confirmation in other populations.

    View details for DOI 10.1007/s10552-012-0100-1

    View details for Web of Science ID 000314063900010

    View details for PubMedID 23208661

  • Atypical prediagnosis Epstein-Barr virus serology restricted to EBV-positive Hodgkin lymphoma BLOOD Levin, L. I., Chang, E. T., Ambinder, R. F., Lennette, E. T., Rubertone, M. V., Mann, R. B., Borowitz, M., Weir, E. G., Abbondanzo, S. L., Mueller, N. E. 2012; 120 (18): 3750-3755

    Abstract

    An altered anti-Epstein-Barr virus (EBV) serologic profile preceding diagnosis is associated with an increased risk of Hodgkin lymphoma. It is unknown whether this atypical pattern predicts Hodgkin lymphoma risk further subdivided by determination of EBV in tumor cells. A nested case-control study of 128 incident Hodgkin lymphoma cases and 368 matched controls from active-duty military personnel with archived serum in the US Department of Defense Serum Repository was conducted to determine whether a panel of anti-EBV antibody titers differed in EBV(+) and EBV(-) Hodgkin lymphoma. Among 40 EBV(+) Hodgkin lymphoma cases and matched controls, statistically significant increased risks were associated with elevated anti-EBV VCA IgG antibody titers (relative risk = 3.1; 95% confidence interval [CI], 1.1-8.7), and an anti-EBNA-1/anti-EBNA-2 antibody ratio ? 1.0 versus > 1.0 (relative risk = 4.7; 95% CI, 1.6-13.8). In contrast, no significant associations were found among 88 EBV(-) Hodgkin lymphoma cases relative to their matched controls. In case-case analysis, EBV(+) disease was significantly associated with a low anti-EBNA-1/anti-EBNA-2 antibody ratio. This distinctive serologic response to EBV latent antigens, indicative of immune dysfunction in other clinical settings, is associated with an increased risk of developing EBV(+) but not EBV(-) Hodgkin lymphoma.

    View details for DOI 10.1182/blood-2011-12-390823

    View details for Web of Science ID 000311624800018

    View details for PubMedID 22972983

  • Nonsteroidal anti-inflammatory drugs and the risk of skin cancer: a population-based case-control study. Cancer Johannesdottir, S. A., Chang, E. T., Mehnert, F., Schmidt, M., Olesen, A. B., Sørensen, H. T. 2012; 118 (19): 4768-4776

    Abstract

    Nonsteroidal anti-inflammatory drugs (NSAIDs) may prevent the development of cancer by inhibiting cyclooxygenase (COX) enzymes, which are involved in carcinogenesis. Therefore, the authors of this report examined the association between NSAID use and the risk of squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and malignant melanoma (MM).From 1991 through 2009, all incident cases of SCC (n = 1974), BCC (n = 13,316), and MM (n = 3242) in northern Denmark were identified. Approximately 10 population controls (n = 178,655) were matched to each case by age, gender, and county of residence. The use of aspirin, other nonselective NSAIDs, or selective COX-2 inhibitors was ascertained through a prescription database. Conditional logistic regression analyses adjusted for potential confounders were used to compute odds ratios as estimates of incidence rate ratios (IRRs).For NSAIDs overall, ever use (>2 prescriptions) compared with nonuse (≤2 prescriptions) was associated with a decreased risk of SCC (IRR, 0.85; 95% confidence interval [CI], 0.76-0.94) and MM (IRR, 0.87; 95% CI, 0.80-0.95), especially for long-term use (≥7 years) and high-intensity use (>25% prescription coverage during the total duration of use). NSAID use was not associated with a reduced risk of BCC overall (IRR, 0.97; 95% CI, 0.93-1.01), but the risk of BCC at sites other than the head and neck was reduced in association with long-term use (IRR, 0.85; 95% CI, 0.76-0.95) and high-intensity use (IRR, 0.79; 95% CI, 0.69-0.91). All estimates of reduced risk were driven primarily by the use of nonselective NSAIDs and older COX-2 inhibitors (diclofenac, etodolac, and meloxicam).The current results indicated that NSAID use may decrease the risk of SCC and MM.

    View details for DOI 10.1002/cncr.27406

    View details for PubMedID 22644960

  • Gastric Cancer Incidence among Hispanics in California: Patterns by Time, Nativity, and Neighborhood Characteristics CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Gomez, S. L., Fish, K., Schupp, C. W., Parsonnet, J., DeRouen, M. C., Keegan, T. H., Clarke, C. A., Glaser, S. L. 2012; 21 (5): 709-719

    Abstract

    Better understanding about gastric cancer incidence patterns among Hispanics by birthplace, socioeconomic status (SES), and acculturation can improve preventive strategies and disease models.Incidence rates, rate ratios, and estimated annual percent change (EAPC) in rates of anatomic and histologic subtype-specific gastric cancer were calculated by age, sex, and nativity among Hispanics using California Cancer Registry data from 1988 through 2004. Incidence rates in 1998 to 2002 were compared by neighborhood SES and Hispanic enclave status according to 2000 US Census data.Incidence rates of diffuse gastric cancer increased from 1988 through 2004 among foreign-born Hispanic men (EAPC: 3.5%, 95% CI: 1.5%-5.5%) and U.S.-born Hispanic women (EAPC: 3.0%, 95% CI: 0.7%-5.3%). During the same time period, incidence rates of intestinal gastric cancer declined significantly and both cardia and noncardia gastric cancer were steady or declined among foreign-born and U.S.-born Hispanic men and women. Noncardia and both intestinal and diffuse gastric cancer were more common in foreign-born than U.S.-born Hispanic men and women, and in those from lower SES, higher enclave neighborhoods. By contrast, among younger and middle-aged Hispanic men, cardia tumors were more common in the U.S.-born than the foreign-born, and in higher SES, lower enclave neighborhoods.Varying gastric cancer risk factors among Hispanic subgroups and increasing rates of diffuse gastric cancer in foreign-born Hispanic men and U.S.-born Hispanic women merit further investigation to identify separate disease etiologies.Age, sex, birthplace, SES, and acculturation modify gastric cancer incidence in Hispanics and should be considered when examining disease risk and prevention.

    View details for DOI 10.1158/1055-9965.EPI-11-1208

    View details for Web of Science ID 000303908200004

    View details for PubMedID 22374991

  • Enigmatic sex disparities in cancer incidence EUROPEAN JOURNAL OF EPIDEMIOLOGY Edgren, G., Liang, L., Adami, H., Chang, E. T. 2012; 27 (3): 187-196

    Abstract

    In this study we aimed to identify cancers where there is a consistent sex disparity, with the goal of identifying unexplained sex disparities that may offer promising opportunities for etiologic research. Age- and sex-specific cancer incidence data from Cancer Incidence in Five Continents, provided by the International Agency for Research on Cancer, were used to calculate incidence rate ratios for 35 cancer sites, comparing men to women, adjusting for attained age, gross domestic product (GDP), and geographical region. Genital cancers and breast cancer were excluded. The consistency of relative risks was examined by GDP and geographical region and, in a subset of longstanding cancer registers, by calendar year. For each cancer site, the sex disparity was broadly classified as plausibly explained by established environmental risk factors, partly explained, or unexplained. Cancer incidence was statistically significantly higher in men than women at 32 of 35 sites, with disparities >2-fold for 15 sites and >4-fold for 5 sites. For nearly all sites, the sex disparity was consistent across GDP groups and geographical regions. However, the incidence rate ratios varied considerably by age at diagnosis. The sex disparity for 13 cancer sites was considered to be entirely unexplained by known risk factors; these sites showed strikingly little variation in the incidence rate ratios over decades. Thus, the basis of many of the largest sex disparities in cancer incidence seems mostly unknown, highlighting the need for intensified research into its origins.

    View details for DOI 10.1007/s10654-011-9647-5

    View details for Web of Science ID 000305218800004

    View details for PubMedID 22212865

  • Racial patterns of extranodal natural killer/T-cell lymphoma, nasal type, in California: a population-based study BRITISH JOURNAL OF HAEMATOLOGY Ai, W. Z., Chang, E. T., Fish, K., Fu, K., Weisenburger, D. D., Keegan, T. H. 2012; 156 (5): 626-632

    Abstract

    In order to investigate whether the clinical behaviour of extranodal natural killer/T-cell lymphoma, nasal type (ENKTL) varies by race within a geographic region, we identified a total of 213 non-Hispanic whites, Hispanics and Asians/Pacific islanders (APIs) diagnosed with ENKTL in the California Cancer Registry between 2001 and 2008. The incidence and outcomes of the disease in these racial groups were analysed. The incidence rates in non-Hispanic whites, Hispanics and APIs were 0.05, 0.18 and 0.23 per 100,000 person-years, respectively, among males; and 0.03, 0.07 and 0.10 per 100,000 person-years, respectively, among females. The overall survival (OS) at 5 years was 28.6% in non-Hispanic whites, 30.4% in Hispanic, and 24.0% in APIs. In multivariate analysis, distant versus local/regional disease (Hazard Ratio [HR]=2.01, 95% confidence interval [CI]: 1.36, 2.96), initial treatment with chemotherapy plus radiotherapy (HR=0.39, 95% CI: 0.22, 0.70) or radiotherapy alone (HR=0.48, 95% CI: 0.23, 0.99) versus no therapy were associated with OS. However, OS was not affected by age, sex, race, chemotherapy alone, socioeconomic status, or human immunodeficiency virus infection. In conclusion, ENKTL is more common and clinically more similar among Hispanics and APIs than non-Hispanic whites with poor outcome in all racial groups.

    View details for DOI 10.1111/j.1365-2141.2011.08982.x

    View details for Web of Science ID 000300971800007

    View details for PubMedID 22188140

  • A nationwide study of aspirin, other non-steroidal anti-inflammatory drugs, and Hodgkin lymphoma risk in Denmark BRITISH JOURNAL OF CANCER Chang, E. T., Froslev, T., Sorensen, H. T., Pedersen, L. 2011; 105 (11): 1776-1782

    Abstract

    We recently found an inverse association between low-dose aspirin use and risk of Hodgkin lymphoma (HL) in northern Denmark. To strengthen the evidence for this association, we expanded the study base to include all of Denmark.Between 1997 and 2009, 1659 incident HL cases were identified in nationwide databases and matched with ?5 population controls on age, sex, and residence. Use of aspirin, selective cyclooxygenase-2 (sCOX-2) inhibitors, and other non-steroidal anti-inflammatory drugs (NSAIDs) from 1995 through 2008 (?1 year before the index date) was ascertained via the Danish National Prescription Database. Odds ratios (ORs) for associations with HL risk were estimated using conditional logistic regression.Ever use (>2 prescriptions) vs never/rare use (?2 prescriptions) of low-dose aspirin was not associated with HL risk, but the association with long-term use for ?7 years vs never/rare use was clearly inverse, although statistically nonsignificantly so (OR=0.65, 95% confidence interval (CI): 0.39-1.09). By contrast, ever use of sCOX-2 inhibitors or other NSAIDs (OR=1.27, 95% CI: 1.10-1.47), especially short-term and low- or medium-intensity use, was associated with elevated HL risk.Our results are consistent with the hypothesis that long-term use of low-dose aspirin, but not other NSAIDs, protects against HL development.

    View details for DOI 10.1038/bjc.2011.443

    View details for Web of Science ID 000297687600023

    View details for PubMedID 22027707

  • Adulthood residential ultraviolet radiation, sun sensitivity, dietary vitamin D, and risk of lymphoid malignancies in the California Teachers Study BLOOD Chang, E. T., Canchola, A. J., Cockburn, M., Lu, Y., Wang, S. S., Bernstein, L., Clarke, C. A., Horn-Ross, P. L. 2011; 118 (6): 1591-1599

    Abstract

    To lend clarity to inconsistent prior findings of an inverse association between ultraviolet radiation (UVR) exposure and risk of lymphoid malignancies, we examined the association of prospectively ascertained residential ambient UVR exposure with risk of non-Hodgkin lymphomas (NHLs), multiple myeloma (MM), and classical Hodgkin lymphoma in the California Teachers Study cohort. Among 121 216 eligible women, 629 were diagnosed with NHL, 119 with MM, and 38 with Hodgkin lymphoma between 1995-1996 and 2007. Cox proportional hazards regression was used to estimate incidence rate ratios (RRs) with 95% confidence intervals (CIs). Residential UVR levels within a 20-km radius were associated with reduced risk of overall NHL (RR for highest vs lowest statewide quartile of minimum UVR [? 5100 vs < 4915 W-h/m(2)], 0.58; 95% CI, 0.42-0.80), especially diffuse large B-cell lymphoma (RR, 0.36; 95% CI, 0.17-0.78) and chronic lymphocytic leukemia/small lymphocytic lymphoma (RR, 0.46; 95% CI, 0.21-1.01), and MM (RR for maximum UVR, 0.57; 95% CI, 0.36-0.90). These associations were not modified by skin sensitivity to sunlight, race/ethnicity, body mass index, or neighborhood socioeconomic status. Dietary vitamin D also was not associated with risk of lymphoid malignancies. These results support a protective effect of routine residential UVR exposure against lymphomagenesis through mechanisms possibly independent of vitamin D.

    View details for DOI 10.1182/blood-2011-02-336065

    View details for Web of Science ID 000293787300026

    View details for PubMedID 21622649

  • Dietary phytocompounds and risk of lymphoid malignancies in the California Teachers Study cohort CANCER CAUSES & CONTROL Chang, E. T., Canchola, A. J., Clarke, C. A., Lu, Y., West, D. W., Bernstein, L., Wang, S. S., Horn-Ross, P. L. 2011; 22 (2): 237-249

    Abstract

    We examined whether dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or specific foods rich in these compounds is associated with reduced risk of B-cell non-Hodgkin lymphoma (NHL), multiple myeloma (MM), or Hodgkin lymphoma (HL) in a large, prospective cohort of women.Between 1995-1996 and 31 December 2007, among 110,215 eligible members of the California Teachers Study cohort, 536 women developed incident B-cell NHL, 104 developed MM, and 34 developed HL. Cox proportional hazards regression, with age as the time scale, was used to estimate adjusted rate ratios (RRs) with 95% confidence intervals (CIs) for risk of lymphoid malignancies.Weak inverse associations with risk of diffuse large B-cell lymphoma were observed for isothiocyanates (RR for ?12.1 vs. <2.7 mcM/day = 0.67, 95% CI: 0.43-1.05) and an antioxidant index measuring hydroxyl radical absorbance capacity (RR for ?2.2 vs. <0.9 ?M Trolox equiv/g/day = 0.68, 95% CI: 0.42-1.10; p (trend) = 0.08). Risk of other NHL subtypes, overall B-cell NHL, MM, or HL was not generally associated with dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or major food sources of these compounds.Isoflavones, lignans, isothiocyanates, and antioxidant compounds are not associated with risk of most B-cell malignancies, but some phytocompounds may decrease the risk of selected subtypes.

    View details for DOI 10.1007/s10552-010-9692-5

    View details for Web of Science ID 000286465000009

    View details for PubMedID 21107674

  • Vitamin D Receptor Genotypes, Ultraviolet Radiation Exposure, and Risk of Non-Hodgkin Lymphoma AMERICAN JOURNAL OF EPIDEMIOLOGY Smedby, K. E., Eloranta, S., Duvefelt, K., Melbye, M., Humphreys, K., Hjalgrim, H., Chang, E. T. 2011; 173 (1): 48-54

    Abstract

    Ultraviolet radiation (UVR) exposure may influence risk of non-Hodgkin lymphoma (NHL) through vitamin D, with antineoplastic effects mediated through the vitamin D receptor (VDR). To explore the role of vitamin D in NHL risk and the potential interaction with UVR, the authors genotyped 10 VDR polymorphisms in 2,448 NHL patients and 1,981 controls from Denmark and Sweden who were recruited in 1999-2002. Odds ratios and 95% confidence intervals were computed with logistic regression. P values were 2-sided. Most VDR variants (e.g., rs731236/TaqI, rs15444410/BsmI) were not associated with overall risk of NHL, but there was some evidence of a positive association between rs4760655 and follicular lymphoma risk (nominal P(trend) = 0.004, corrected P(trend) = 0.24). There was no support for an effect of interaction between VDR variants and UVR exposure on risk of overall NHL or B-cell lymphoma subtypes. However, there was some evidence that rs731236 altered associations between UVR and T-cell NHL risk; while increasing UVR frequency lowered T-cell NHL risk among rs731236 TT carriers, an elevated risk was observed among rs731236 CC carriers (nominal P(interaction) ? 0.008, corrected P(interaction) ? 0.12). VDR does not appear to harbor major determinants of NHL risk, except perhaps for follicular lymphoma. Possible heterogeneity in effects of UVR exposure on T-cell lymphoma risk by VDR rs731236 genotype merits further investigation.

    View details for DOI 10.1093/aje/kwq340

    View details for Web of Science ID 000285412200005

    View details for PubMedID 21076051

  • Alcohol Consumption Over Time and Risk of Lymphoid Malignancies in the California Teachers Study Cohort AMERICAN JOURNAL OF EPIDEMIOLOGY Chang, E. T., Clarke, C. A., Canchola, A. J., Lu, Y., Wang, S. S., Ursin, G., West, D. W., Bernstein, L., Horn-Ross, P. L. 2010; 172 (12): 1373-1383

    Abstract

    Several previous studies found inverse associations between alcohol consumption and risk of non-Hodgkin lymphoma (NHL) and multiple myeloma. However, most studies were retrospective, and few distinguished former drinkers or infrequent drinkers from consistent nondrinkers. Therefore, the authors investigated whether history of alcohol drinking affected risks of NHL and multiple myeloma among 102,721 eligible women in the California Teachers Study, a prospective cohort study in which 496 women were diagnosed with B-cell NHL and 101 were diagnosed with multiple myeloma between 1995-1996 and December 31, 2007. Incidence rate ratios and 95% confidence intervals were estimated using Cox proportional hazards regression. Risk of all types of B-cell NHL combined or multiple myeloma was not associated with self-reported past consumption of alcohol, beer, wine, or liquor at ages 18-22 years, at ages 30-35 years, or during the year before baseline. NHL subtypes were inconsistently associated with alcohol intake. However, women who were former alcohol drinkers at baseline were at elevated risk of overall B-cell NHL (rate ratio = 1.46, 95% confidence interval: 1.08, 1.97) and follicular lymphoma (rate ratio = 1.81, 95% confidence interval: 1.00, 3.28). The higher risk among former drinkers emphasizes the importance of classifying both current and past alcohol consumption and suggests that factors related to quitting drinking, rather than alcohol itself, may increase B-cell NHL risk.

    View details for DOI 10.1093/aje/kwq309

    View details for Web of Science ID 000285193200008

    View details for PubMedID 20952595

  • Disparities in Liver Cancer Incidence by Nativity, Acculturation, and Socioeconomic Status in California Hispanics and Asians CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Yang, J., Alfaro-Velcamp, T., So, S. K., Glaser, S. L., Gomez, S. L. 2010; 19 (12): 3106-3118

    Abstract

    Asians and Hispanics have the highest incidence rates of liver cancer in the United States, but little is known about how incidence patterns in these largely immigrant populations vary by nativity, acculturation, and socioeconomic status (SES). Such variations can identify high-priority subgroups for prevention and monitoring.Incidence rates and rate ratios (IRR) by nativity among 5,400 Hispanics and 5,809 Asians diagnosed with liver cancer in 1988-2004 were calculated in the California Cancer Registry. Neighborhood ethnic enclave status and SES were classified using 2000 U.S. Census data for cases diagnosed in 1998-2002.Foreign-born Hispanic males had significantly lower liver cancer incidence rates than U.S.-born Hispanic males in 1988-2004 (e.g., IRR = 0.54, 95% confidence interval [CI] = 0.50-0.59 in 1997-2004), whereas foreign-born Hispanic females had significantly higher rates in 1988-1996 (IRR = 1.42, 95% CI = 1.18-1.71), but not 1997-2004. Foreign-born Asian males and females had up to 5-fold higher rates than the U.S.-born. Among Hispanic females, incidence rates were elevated by 21% in higher-enclave versus lower-enclave neighborhoods, and by 24% in lower- versus higher-SES neighborhoods. Among Asian males, incidence rates were elevated by 23% in higher-enclave neighborhoods and by 21% in lower-SES neighborhoods. In both racial/ethnic populations, males and females in higher-enclave, lower-SES neighborhoods had higher incidence rates.Nativity, residential enclave status, and neighborhood SES characterize Hispanics and Asians with significantly unequal incidence rates of liver cancer, implicating behavioral or environmental risk factors and revealing opportunities for prevention.Liver cancer control efforts should especially target foreign-born Asians, U.S.-born Hispanic men, and residents of lower-SES ethnic enclaves.

    View details for DOI 10.1158/1055-9965.EPI-10-0863

    View details for Web of Science ID 000285285900012

    View details for PubMedID 20940276

  • Aspirin and Other Nonsteroidal Anti-inflammatory Drugs in Relation to Hodgkin Lymphoma Risk in Northern Denmark CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Cronin-Fenton, D. P., Friis, S., Hjalgrim, H., Sorensen, H. T., Pedersen, L. 2010; 19 (1): 59-64

    Abstract

    There are few known modifiable risk factors for Hodgkin lymphoma, but the recent finding of an inverse association between routine regular-strength aspirin use and Hodgkin lymphoma risk suggests that aspirin may protect against Hodgkin lymphoma development. To further investigate this association using prospectively collected data, we conducted a population-based case-control study in northern Denmark. A total of 478 incident Hodgkin lymphoma cases were identified in nationwide health-care databases from 1991 to 2008. Ten population controls were matched to each case on age, sex, and county using risk-set sampling. Use of aspirin, selective cyclooxygenase-2 inhibitors, and other nonsteroidal anti-inflammatory drugs (NSAIDs) from 1989 to 2007 was ascertained by linkage to a population-based prescription database. Conditional logistic regression was used to estimate odds ratios for associations between medication use and risk of Hodgkin lymphoma. The odds ratio (95% confidence interval) for ever use (>2 prescriptions) compared with never/rare use (< or =2 prescriptions) of low-dose aspirin was 0.7 (0.5-1.2). The association with low-dose aspirin use did not vary appreciably by recentness, duration, or intensity of use. Recent use (>2 prescriptions in the 1-2 years before the index date), short-term use (<7 years), and medium/high-intensity use (> or =25% of duration of use covered by prescription) of selective cyclooxygenase-2 inhibitors or other NSAIDs was associated with increased Hodgkin lymphoma risk possibly due to prodromal symptoms among cases. In conclusion, our results provide some evidence of a protective effect of low-dose aspirin, but not other NSAIDs, against Hodgkin lymphoma development.

    View details for DOI 10.1158/1055-9965.EPI-09-0909

    View details for Web of Science ID 000273586700007

    View details for PubMedID 20056623

  • How do social factors explain outcomes in non-small-cell lung cancer among hispanics in california? Explaining the Hispanic paradox. Journal of clinical oncology Patel, M. I., Schupp, C. W., Gomez, S. L., Chang, E. T., Wakelee, H. A. 2013; 31 (28): 3572-3578

    Abstract

    Hispanics in the United States have lower age-adjusted mortality resulting from non-small-cell lung cancer (NSCLC) compared with non-Hispanic whites (NHWs). The purpose of this study was to evaluate individual, clinical, and neighborhood factors in survival among Hispanics with NSCLC.We performed a retrospective analysis of NHWs and Hispanics with NSCLC between 1998 and 2007 in the California Cancer Registry (follow-up to December 2009). Kaplan-Meier curves depict survival by nativity for Hispanics with NSCLC. Cox proportional hazards models estimated hazard of mortality by race with adjustment for individual (age, sex, marital status), clinical (histologic grade, surgery, irradiation, chemotherapy), and neighborhood factors (neighborhood socioeconomic status, ethnic enclave).We included 14,280 Hispanic patients with NSCLC. Foreign-born Hispanics had 15% decreased risk of disease-specific mortality resulting from NSCLC compared with NHWs (hazard ratio [HR], 0.85; 95% CI, 0.83 to 0.88) after adjustment for individual, clinical, and neighborhood factors. After adjustment for individual factors, compared with US-born Hispanics, foreign-born Hispanics had 10% decreased risk of disease-specific mortality (HR, 0.90; 95% CI, 0.87 to 0.96). Clinical and neighborhood factors slightly moderated the survival benefit for foreign-born patients. A modestly more pronounced survival advantage was seen for foreign-born Hispanics living in low socioeconomic and high Hispanic enclave neighborhoods as compared with US-born Hispanics (HR, 0.86; 95% CI, 0.81 to 0.90).Foreign-born Hispanics with NSCLC have a decreased risk of disease-specific mortality compared with NHWs and US-born Hispanics with NSCLC. Neighborhood factors slightly moderate this survival advantage. This survival advantage is slightly more pronounced in lower socioeconomic and higher Hispanic enclave neighborhoods.

    View details for DOI 10.1200/JCO.2012.48.6217

    View details for PubMedID 23960183

  • How do social factors explain outcomes in non-small-cell lung cancer among hispanics in california? Explaining the Hispanic paradox. Journal of clinical oncology Patel, M. I., Schupp, C. W., Gomez, S. L., Chang, E. T., Wakelee, H. A. 2013; 31 (28): 3572-3578

    Abstract

    Hispanics in the United States have lower age-adjusted mortality resulting from non-small-cell lung cancer (NSCLC) compared with non-Hispanic whites (NHWs). The purpose of this study was to evaluate individual, clinical, and neighborhood factors in survival among Hispanics with NSCLC.We performed a retrospective analysis of NHWs and Hispanics with NSCLC between 1998 and 2007 in the California Cancer Registry (follow-up to December 2009). Kaplan-Meier curves depict survival by nativity for Hispanics with NSCLC. Cox proportional hazards models estimated hazard of mortality by race with adjustment for individual (age, sex, marital status), clinical (histologic grade, surgery, irradiation, chemotherapy), and neighborhood factors (neighborhood socioeconomic status, ethnic enclave).We included 14,280 Hispanic patients with NSCLC. Foreign-born Hispanics had 15% decreased risk of disease-specific mortality resulting from NSCLC compared with NHWs (hazard ratio [HR], 0.85; 95% CI, 0.83 to 0.88) after adjustment for individual, clinical, and neighborhood factors. After adjustment for individual factors, compared with US-born Hispanics, foreign-born Hispanics had 10% decreased risk of disease-specific mortality (HR, 0.90; 95% CI, 0.87 to 0.96). Clinical and neighborhood factors slightly moderated the survival benefit for foreign-born patients. A modestly more pronounced survival advantage was seen for foreign-born Hispanics living in low socioeconomic and high Hispanic enclave neighborhoods as compared with US-born Hispanics (HR, 0.86; 95% CI, 0.81 to 0.90).Foreign-born Hispanics with NSCLC have a decreased risk of disease-specific mortality compared with NHWs and US-born Hispanics with NSCLC. Neighborhood factors slightly moderate this survival advantage. This survival advantage is slightly more pronounced in lower socioeconomic and higher Hispanic enclave neighborhoods.

    View details for DOI 10.1200/JCO.2012.48.6217

    View details for PubMedID 23960183

  • Cigarette smoking and risk of Hodgkin lymphoma and its subtypes: a pooled analysis from the International Lymphoma Epidemiology Consortium (InterLymph). Annals of oncology Kamper-Jørgensen, M., Rostgaard, K., Glaser, S. L., ZAHM, S. H., Cozen, W., Smedby, K. E., Sanjosé, S., Chang, E. T., Zheng, T., La Vecchia, C., Serraino, D., Monnereau, A., Kane, E. V., Miligi, L., Vineis, P., Spinelli, J. J., McLaughlin, J. R., Pahwa, P., Dosman, J. A., Vornanen, M., Foretova, L., Maynadie, M., Staines, A., Becker, N., Nieters, A., Brennan, P., Boffetta, P., Cocco, P., Hjalgrim, H. 2013; 24 (9): 2245-2255

    Abstract

    The etiology of Hodgkin lymphoma (HL) remains incompletely characterized. Studies of the association between smoking and HL have yielded ambiguous results, possibly due to differences between HL subtypes.Through the InterLymph Consortium, 12 case-control studies regarding cigarette smoking and HL were identified. Pooled analyses on the association between smoking and HL stratified by tumor histology and Epstein-Barr virus (EBV) status were conducted using random effects models adjusted for confounders. Analyses included 3335 HL cases and 14 278 controls.Overall, 54.5% of cases and 57.4% of controls were ever cigarette smokers. Compared with never smokers, ever smokers had an odds ratio (OR) of HL of 1.10 [95% confidence interval (CI) 1.01-1.21]. This increased risk reflected associations with mixed cellularity cHL (OR = 1.60, 95% CI 1.29-1.99) and EBV-positive cHL (OR = 1.81, 95% CI 1.27-2.56) among current smokers, whereas risk of nodular sclerosis (OR = 1.09, 95% CI 0.90-1.32) and EBV-negative HL (OR = 1.02, 95% CI 0.72-1.44) was not increased.These results support the notion of etiologic heterogeneity between HL subtypes, highlighting the need for HL stratification in future studies. Even if not relevant to all subtypes, our study emphasizes that cigarette smoking should be added to the few modifiable HL risk factors identified.

    View details for DOI 10.1093/annonc/mdt218

    View details for PubMedID 23788758

  • Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia NATURE GENETICS Berndt, S. I., Skibola, C. F., Joseph, V., Camp, N. J., Nieters, A., Wang, Z., Cozen, W., Monnereau, A., Wang, S. S., Kelly, R. S., Lan, Q., Teras, L. R., Chatterjee, N., Chung, C. C., Yeager, M., Brooks-Wilson, A. R., Hartge, P., Purdue, M. P., Birmann, B. M., Armstrong, B. K., Cocco, P., Zhang, Y., Severi, G., Zeleniuch-Jacquotte, A., Lawrence, C., Burdette, L., Yuenger, J., Hutchinson, A., Jacobs, K. B., Call, T. G., Shanafelt, T. D., Novak, A. J., Kay, N. E., Liebow, M., Wang, A. H., Smedby, K. E., Adami, H., Melbye, M., Glimelius, B., Chang, E. T., Glenn, M., Curtin, K., Cannon-Albright, L. A., Jones, B., Diver, W. R., Link, B. K., Weiner, G. J., Conde, L., Bracci, P. M., Riby, J., Holly, E. A., Smith, M. T., Jackson, R. D., Tinker, L. F., Benavente, Y., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., McKay, J., Staines, A., Rabe, K. G., Achenbach, S. J., Vachon, C. M., Goldin, L. R., Strom, S. S., Lanasa, M. C., Spector, L. G., Leis, J. F., Cunningham, J. M., Weinberg, J. B., Morrison, V. A., Caporaso, N. E., Norman, A. D., Linet, M. S., De Roos, A. J., Morton, L. M., Severson, R. K., Riboli, E., Vineis, P., Kaaks, R., Trichopoulos, D., Masala, G., Weiderpass, E., Chirlaque, M., Vermeulen, R. C., Travis, R. C., Giles, G. G., Albanes, D., Virtamo, J., Weinstein, S., Clavel, J., Zheng, T., Holford, T. R., Offit, K., Zelenetz, A., Klein, R. J., Spinelli, J. J., Bertrand, K. A., Laden, F., Giovannucci, E., Kraft, P., Kricker, A., Turner, J., Vajdic, C. M., Ennas, M. G., Ferri, G. M., Miligi, L., Liang, L., Sampson, J., Crouch, S., Park, J., North, K. E., Cox, A., Snowden, J. A., Wright, J., Carracedo, A., Lopez-Otin, C., Bea, S., Salaverria, I., Martin-Garcia, D., Campo, E., Fraumeni, J. F., de Sanjose, S., Hjalgrim, H., Cerhan, J. R., Chanock, S. J., Rothman, N., Slager, S. L. 2013; 45 (8): 868-U202

    Abstract

    Genome-wide association studies (GWAS) have previously identified 13 loci associated with risk of chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL). To identify additional CLL susceptibility loci, we conducted the largest meta-analysis for CLL thus far, including four GWAS with a total of 3,100 individuals with CLL (cases) and 7,667 controls. In the meta-analysis, we identified ten independent associated SNPs in nine new loci at 10q23.31 (ACTA2 or FAS (ACTA2/FAS), P = 1.22 × 10(-14)), 18q21.33 (BCL2, P = 7.76 × 10(-11)), 11p15.5 (C11orf21, P = 2.15 × 10(-10)), 4q25 (LEF1, P = 4.24 × 10(-10)), 2q33.1 (CASP10 or CASP8 (CASP10/CASP8), P = 2.50 × 10(-9)), 9p21.3 (CDKN2B-AS1, P = 1.27 × 10(-8)), 18q21.32 (PMAIP1, P = 2.51 × 10(-8)), 15q15.1 (BMF, P = 2.71 × 10(-10)) and 2p22.2 (QPCT, P = 1.68 × 10(-8)), as well as an independent signal at an established locus (2q13, ACOXL, P = 2.08 × 10(-18)). We also found evidence for two additional promising loci below genome-wide significance at 8q22.3 (ODF1, P = 5.40 × 10(-8)) and 5p15.33 (TERT, P = 1.92 × 10(-7)). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism.

    View details for DOI 10.1038/ng.2652

    View details for Web of Science ID 000322374900008

    View details for PubMedID 23770605

  • Lifestyle factors, autoimmune disease and family history in prognosis of non-hodgkin lymphoma overall and subtypes INTERNATIONAL JOURNAL OF CANCER Simard, J. F., Baecklund, F., Chang, E. T., Baecklund, E., Hjalgrim, H., Adami, H., Glimelius, B., Smedby, K. E. 2013; 132 (11): 2659-2666

    Abstract

    Lifestyle factors and medical history are known to influence risk of non-Hodgkin lymphoma (NHL). Whether these factors affect the prognosis of NHL, especially its subtypes, is unclear. To investigate this, the association between these factors and all-cause and lymphoma-related mortality was assessed in a population-based cohort of 1,523 Swedish NHL patients included in the Scandinavian Lymphoma Etiology study in 1999-2002. Participants contributed time from NHL diagnosis until death or October 1, 2010, with virtually complete follow-up through linkage to the Swedish Cause of Death Register. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using stratified and multivariable-adjusted Cox regression models. During a median follow-up of 8.8 years, 670 patients (44%) died, with the majority of deaths attributed to lymphoma (86%). Current versus never smoking at diagnosis was associated with increased rate of all-cause death for all NHL (HR = 1.5, 1.2-1.8) and diffuse large B-cell lymphoma (HR = 1.8, 1.2-2.7). Low educational level (HR = 1.3, 1.1-1.7, <9 vs. >12 years) and NHL risk-associated autoimmune disease (HR = 1.4, 1.0-1.8) were associated with death for all NHL combined. However, evidence of an association with lymphoma-related death was limited. Body mass index, recent sunbathing and family history of hematopoietic malignancy were not consistently associated with death after NHL or its specific subtypes. These results add to the evidence that cigarette smoking, socioeconomic status and certain autoimmune diseases affect survival after NHL. Further investigations are needed to determine how these factors should be incorporated into clinical prognostic assessment.

    View details for DOI 10.1002/ijc.27944

    View details for Web of Science ID 000316824000022

    View details for PubMedID 23160780

  • Rituximab use and survival after diffuse large B-cell or follicular lymphoma: a population-based study LEUKEMIA & LYMPHOMA Keegan, T. H., Moy, L. M., Foran, J. M., Alizadeh, A. A., Chang, E. T., Shema, S. J., Schupp, C. W., Clarke, C. A., Glaser, S. L. 2013; 54 (4): 743-751

    Abstract

    To determine whether reported socioeconomic disparities in survival might be related to treatment, we examined patient and tumor characteristics associated with receipt of rituximab and survival in the National Cancer Institute's Patterns of Care Studies (2003 and 2008) for patients with diffuse large B-cell (DLBCL) and follicular (FL) lymphoma. Patients with DLBCL (n = 1192) were less likely to receive rituximab if they were older, black or Asian, lacked private medical insurance, had impaired performance status, had no lactate dehydrogenase measurements or were diagnosed with stage I disease. Patients with FL (n = 476) were less likely to receive rituximab if they were unmarried or non-Hispanic white. Receipt of rituximab did not differ by neighborhood median income. Treatment with rituximab was associated with better survival for patients with DLBCL, but not patients with FL. Lower rituximab use in patients with DLBCL without private insurance suggests that previously identified socioeconomic disparities in survival may, in part, be explained by receipt of rituximab.

    View details for DOI 10.3109/10428194.2012.727415

    View details for Web of Science ID 000315898100015

    View details for PubMedID 22957852

  • Subtype of dietary fat in relation to risk of Hodgkin lymphoma: a population-based case-control study in Connecticut and Massachusetts CANCER CAUSES & CONTROL Gao, Y., Li, Q., Bassig, B. A., Chang, E. T., Dai, M., Qin, Q., Zhang, Y., Zheng, T. 2013; 24 (3): 485-494

    Abstract

    Few epidemiological studies have examined the relationship between dietary fat, which may affect immune function and risk of Hodgkin lymphoma (HL). The aim of this study was to test the hypothesis that high dietary intake of fat and specific subtypes of fat is associated with the risk of HL among 486 HL cases and 630 population-based controls recruited between 1997 and 2000 in Connecticut and Massachusetts. Unconditional logistic regression was used to calculate odds ratios (ORs) and 95 % confidence intervals (CIs) stratified by age and gender. Among younger adults, HL risk was significantly and positively associated with higher intake of saturated fat [ORs for increasing quartiles = 1.3, 1.8, and 2.1; p trend = 0.04] and negatively associated with higher intake of monounsaturated fat [ORs for increasing quartiles = 0.5, 0.5, and 0.4; p trend = 0.03), after adjustment for potential confounders including lifestyle and other dietary factors. The associations with saturated fat (ORs for increasing quartile = 2.4, 3.2, and 4.4; p trend < 0.01] and monounsaturated fat (ORs for increasing quartile = 0.3, 0.6, and 0.3; p trend = 0.04) were most apparent in younger women, whereas there was no significant association between intake of total fat or any type of fat and risk of HL in older females or younger or older males. These findings show that the associations between dietary fat and risk of HL may vary by gender and age and require confirmation in other populations.

    View details for DOI 10.1007/s10552-012-0136-2

    View details for Web of Science ID 000314976900008

    View details for PubMedID 23314676

  • Education and counseling of pregnant patients with chronic hepatitis B: perspectives from obstetricians and perinatal nurses in santa clara county, california. Asian Pacific journal of cancer prevention Yang, E. J., Cheung, C. M., So, S. K., Chang, E. T., Chao, S. D. 2013; 14 (3): 1707-1713

    Abstract

    Background: This study aimed to better understand the barriers to perinatal hepatitis B prevention and to identify the reasons for poor hepatitis B knowledge and delivery of education to hepatitis B surface-antigen- positive pregnant women among healthcare providers in Santa Clara County, California. Materials and Methods: Qualitative interviews were conducted with 16 obstetricians and 17 perinatal nurses in Santa Clara County, California, which has one of the largest populations in the United States at high risk for perinatal hepatitis B transmission. Results: Most providers displayed a lack of self-efficacy attributed to insufficient hepatitis B training and education. They felt discouraged from counseling and educating their patients because of a lack of resources and discouraging patient attitudes such as stigma and apathy. Providers called for institutional changes from the government, hospitals, and nonprofit organizations to improve care for patients with chronic hepatitis B. Conclusions: Early and continuing provider training, increased public awareness, and development of comprehensive resources and new programs may contribute to reducing the barriers for health care professionals to provide counseling and education to pregnant patients with chronic hepatitis B infection.

    View details for PubMedID 23679261

  • Anthropometric, behavioral, and female reproductive factors and risk of multiple myeloma: a pooled analysis. Cancer causes & control : CCC Wang, S. S., Voutsinas, J., Chang, E. T., Clarke, C. A., Lu, Y., Ma, H., West, D., Lacey, J. V., Bernstein, L. 2013

    Abstract

    BACKGROUND: Risk of developing multiple myeloma (MM) rises with age and is greater among men and blacks than among women and whites, respectively, and possibly increased among obese persons. Other risk factors remain poorly understood. By pooling data from two complementary epidemiologic studies, we assessed whether obesity, smoking, or alcohol consumption alters MM risk and whether female reproductive history might explain the lower occurrence of MM in females than in males. METHODS: The Los Angeles County MM Case-Control Study (1985-1992) included 278 incident cases and 278 controls, matched on age, sex, race, and neighborhood of residence at case's diagnosis. We estimated MM risk using conditional logistic regression to calculate odds ratios (ORs) and 95 % confidence intervals (CIs). In the prospective California Teachers Study (CTS), 152 women were diagnosed with incident MM between 1995 and 2009; we calculated hazard ratios using Cox proportional hazards analysis. Data from the two studies were pooled using a stratified, nested case-control sampling scheme (10:1 match) for the CTS; conditional logistic regression among 430 cases and 1,798 matched controls was conducted. RESULTS: Obesity and smoking were not associated with MM risk in the individual or combined studies. Alcohol consumption was associated with decreased MM risk among whites only (pooled OR = 0.66, 95 % CI = 0.49-0.90) for ever versus never drinking. Higher gravidity and parity were associated with increased MM risk, with pooled ORs of 1.38 (95 % CI = 1.01-1.90) for ?3 versus 1-2 pregnancies and 1.50 (95 % CI = 1.09-2.06) for ?3 versus 1-2 live births. CONCLUSIONS: Female reproductive history may modestly alter MM risk, but appears unlikely to explain the sex disparity in incidence. Further investigation in consortial efforts is warranted.

    View details for PubMedID 23568533

  • Allergy-associated symptoms in relation to childhood non-Hodgkin's as contrasted to Hodgkin's lymphomas: A case-control study in Greece and meta-analysis EUROPEAN JOURNAL OF CANCER Dikalioti, S. K., Chang, E. T., Dessypris, N., Papadopoulou, C., Skenderis, N., Pourtsidis, A., Moschovi, M., Polychronopoulou, S., Athanasiadou-Piperopoulou, F., Sidi, V., Kalmanti, M., Petridou, E. T. 2012; 48 (12): 1860-1866

    Abstract

    An increase of the prevalence of childhood allergic diseases and the incidence of childhood Hodgkin's (HL) and non-Hodgkin's lymphoma (NHL) were reported in the late 20th century. Among adults, several studies point to an inverse association with lymphoma; it remains to be confirmed whether allergy is also related to childhood lymphomas and whether the association, if any, is of an aetiologic nature. Between 1996 and 2008, 277 children (aged 0-14 years) with HL (N = 111) or NHL (N = 166) were enrolled in Nationwide Registry for Childhood Hematological Malignancies (NARECHEM), a Greek hospital-based-registry of childhood hematological malignancies. Hospital controls were individually matched to cases on age and sex. Multivariate conditional logistic regression was used to estimate odds ratios (ORs) with 95%confidence intervals (CIs) for associations of allergic diseases and other covariates with childhood HL or NHL risk. Subsequently, we combined our results with those of a French case-control study in a meta-analysis amounting to a total of 330 NHL cases/1478 controls and 239 HL cases/959 controls. After controlling for sociodemographic, perinatal and environmental factors, childhood NHL was less prevalent among children with allergy-associated symptoms overall (OR:0.50, 95%CI:0.27-0.92) or a history of asthma (OR:0.43, 95%CI:0.21-0.88). By contrast, allergy did not seem to be associated with childhood HL risk, although statistical power was limited. Fewer seaside holidays and higher birth weight were also associated with increased childhood NHL risk. The combined OR of the two studies for the association of asthma with NHL risk was: 0.52, 95%CI:0.32-0.84, whereas for HL: 0.86, 95%CI:0.51-1.45. Allergy seems to be strongly and inversely associated with childhood NHL. It remains to be elucidated in future investigations comprising larger populations, focusing on specific disease subtypes and employing more pertinent study-designs, whether this association is genuinely protective.

    View details for DOI 10.1016/j.ejca.2011.12.010

    View details for Web of Science ID 000306611200014

    View details for PubMedID 22230747

  • Low Levels of Knowledge and Preventive Practices Regarding Vertical Hepatitis B Transmission among Perinatal Nurses JOGNN-JOURNAL OF OBSTETRIC GYNECOLOGIC AND NEONATAL NURSING Chao, S. D., Cheung, C. M., Yang, E. J., So, S. K., Chang, E. T. 2012; 41 (4): 494-505

    Abstract

    To evaluate current levels of hepatitis-B-related knowledge and clinical practice among perinatal nurses.Cross-sectional study.Santa Clara County, California, home to one of the largest U.S. populations at risk of perinatal hepatitis B transmission.Perinatal nurses (N = 518) from eight birthing hospitals.In 2008-2010, nurses completed a baseline survey evaluating existing hepatitis-B-related knowledge and preventive clinical practices, participated in an educational seminar, received instructional materials about hepatitis B, and completed a follow-up knowledge survey.Eighty percent of perinatal nurses had provided health care to a pregnant woman with chronic hepatitis B, but only 51% routinely provided patients with educational information about hepatitis B. While 75% routinely informed patients about effective methods to prevent mother-to-child transmission, only a small minority (17-34%) educated infected women about standard recommendations for protecting themselves and household members. One fourth or fewer nurses correctly answered most questions about hepatitis B prevalence, risks, and symptoms. After the educational seminar, knowledge increased statistically significantly.Existing knowledge about hepatitis B is limited, and nationally recommended preventive clinical practices are commonly overlooked by perinatal nurses. This lack of knowledge and preventive care represents a noteworthy gap and an opportunity for targeted training and education to improve perinatal hepatitis B prevention and medical management of infected mothers.

    View details for DOI 10.1111/j.1552-6909.2012.01379.x

    View details for Web of Science ID 000306476300006

    View details for PubMedID 22697047

  • A model program for hepatitis B vaccination and education of schoolchildren in rural China INTERNATIONAL JOURNAL OF PUBLIC HEALTH Chen, J. J., Chang, E. T., Chen, Y., Bailey, M. B., So, S. K. 2012; 57 (3): 581-588

    Abstract

    Incomplete hepatitis B virus (HBV) vaccine coverage and poor HBV-related knowledge in China leave millions of children unprotected from this life-threatening infection. To address these gaps, a pilot program for HBV education and vaccination was launched in rural China.In 2006, public and private organizations in the US and China collaborated to provide HBV education and vaccination to 55,000 school-age children in the remote, highly HBV-endemic area of Qinghai Province. The impact of the educational program on HBV-related knowledge was evaluated among more than 2,800 elementary school students.Between September 2006 and March 2007, the three-shot hepatitis B vaccine series was administered to 54,680 students, with a completion rate of 99.4%. From low pre-existing knowledge levels, classroom educational sessions statistically significantly increased knowledge about HBV risks, symptoms, transmission, and prevention.This program offers an effective and sustainable model for HBV catch-up vaccination and education that can be replicated throughout China, as well as in other underserved HBV-endemic regions, as a strategy to reduce chronic HBV infection, liver failure, and liver cancer.

    View details for DOI 10.1007/s00038-011-0289-x

    View details for Web of Science ID 000304446100015

    View details for PubMedID 21845405

  • Risk factors for hepatocellular carcinoma in patients with chronic liver disease: a case-control study CANCER CAUSES & CONTROL Ha, N. B., Ha, N. B., Ahmed, A., Ayoub, W., Daugherty, T. J., Chang, E. T., Lutchman, G. A., Garcia, G., Cooper, A. D., Keeffe, E. B., Nguyen, M. H. 2012; 23 (3): 455-462

    Abstract

    The majority of data on risk factors (RFs) for hepatocellular carcinoma (HCC) comes from studies involving populations without underlying liver disease. It is important to evaluate RFs for HCC in patients with chronic liver disease since HCC rarely occurs in those without underlying liver disease. We conducted a hospital-based case-control study of 259 incident HCC cases and 781 controls by convenience sampling between 02/2001 and 12/2009 from the liver clinic at Stanford University Medical Center. The study population was 41% White, 14% Hispanic, 3% African American, 40% Asian American, and 2% other race/ethnicity. RFs were examined through medical records and an in-person questionnaire. Alcohol and tobacco use was calculated by cumulative grams of alcohol or cumulative pack(s) of cigarette consumed over one's lifetime. Diabetes mellitus (DM) was defined by random glucose level of ?200 mg/dL. RFs were evaluated using multivariate logistic regression. Independent predictors of HCC risk, after mutual adjustment and additional control for alcohol use, etiology of liver diseases, and DM, included age >40 (OR = 8.5 [2.6-28.3]), male gender (OR = 3.5 [2.2-5.8]), presence of cirrhosis (OR = 2.8 [1.6-4.9]), Asian ethnicity (OR = 2.8 [1.8-4.6]), AFP > 50 (OR = 4.2 [2.6-6.8]), and cumulative lifetime tobacco use of >11,000 packs (OR = 1.7 [1.0-2.9]). Heavy prolonged cigarette smoking, but not alcohol use, was a significant independent predictor for HCC in patients with underlying liver disease. Besides older age, male gender, presence of cirrhosis, and elevated AFP, Asian ethnicity and heavy cumulative tobacco use are strong independent predictors of HCC.

    View details for DOI 10.1007/s10552-012-9895-z

    View details for Web of Science ID 000300891100006

    View details for PubMedID 22258434

  • Nativity and papillary thyroid cancer incidence rates among Hispanic women in California CANCER Horn-Ross, P. L., Chang, E. T., Clarke, C. A., Keegan, T. H., Rull, R. P., Thu Quach, T., Gomez, S. L. 2012; 118 (1): 216-222

    Abstract

    Overall, the incidence of papillary thyroid cancer in Hispanic women residing in the United States (US) is similar to that of non-Hispanic white women. However, little is known as to whether rates in Hispanic women vary by nativity, which may influence exposure to important risk factors.Nativity-specific incidence rates among Hispanic women were calculated for papillary thyroid cancer using data from the California Cancer Registry (CCR) for the period 1988-2004. For the 35% of cases for whom birthplace information was not available from the CCR, nativity was statistically imputed based on age at Social Security number issuance. Population estimates were extracted based on US Census data. Incidence rate ratios (IRRs) and 95% confidence intervals (CIs) were also estimated.In young (age <55 years) Hispanic women, the incidence of papillary thyroid cancer among US-born women (10.65 per 100,000) was significantly greater than that for foreign-born women (6.67 per 100,000; IRR, 1.60 [95% CI, 1.44-1.77]). The opposite pattern was observed in older women. The age-specific patterns showed marked differences by nativity: among foreign-born women, rates increased slowly until age 70 years, whereas among US-born women, incidence rates peaked during the reproductive years. Incidence rates increased over the study period in all subgroups.Incidence rates of papillary thyroid cancer vary by nativity and age among Hispanic women residing in California. These patterns can provide insight for future etiologic investigations of modifiable risk factors for this increasingly common and understudied cancer.

    View details for DOI 10.1002/cncr.26223

    View details for Web of Science ID 000298549700027

    View details for PubMedID 21692062

  • Eight-Signature Classifier for Prediction of Nasopharnyngeal Carcinoma Survival JOURNAL OF CLINICAL ONCOLOGY Wang, H., Sun, B., Zhu, Z., Chang, E. T., To, K., Hwang, J. S., Jiang, H., Kam, M. K., Chen, G., Cheah, S., Lee, M., Liu, Z., Chen, J., Zhang, J., Zhang, H., He, J., Chen, F., Zhu, X., Huang, M., Liao, D., Fu, J., Shao, Q., Cai, M., Du, Z., Yan, L., Hu, C., Ng, H., Wee, J. T., Qian, C., Liu, Q., Ernberg, I., Ye, W., Adami, H., Chan, A. T., Zeng, Y., Shao, J. 2011; 29 (34): 4516-4524

    Abstract

    Currently, nasopharyngeal carcinoma (NPC) prognosis evaluation is based primarily on the TNM staging system. This study aims to identify prognostic markers for NPC.We detected expression of 18 biomarkers by immunohistochemistry in NPC tumors from 209 patients and evaluated the association between gene expression level and disease-specific survival (DSS). We used support vector machine (SVM)--based methods to develop a prognostic classifier for NPC (NPC-SVM classifier). Further validation of the NPC-SVM classifier was performed in an independent cohort of 1,059 patients.The NPC-SVM classifier integrated patient sex and the protein expression level of seven genes, including Epstein-Barr virus latency membrane protein 1, CD147, caveolin-1, phospho-P70S6 kinase, matrix metalloproteinase 11, survivin, and secreted protein acidic and rich in cysteine. The NPC-SVM classifier distinguished patients with NPC into low- and high-risk groups with significant differences in 5-year DSS in the evaluated patients (87% v 37.7%; P < .001) in the validation cohort. In multivariate analysis adjusted for age, TNM stage, and histologic subtype, the NPC-SVM classifier was an independent predictor of 5-year DSS in the evaluated patients (hazard ratio, 4.9; 95% CI, 3.0 to 7.9) in the validation cohort.As a powerful predictor of 5-year DSS among patients with NPC, the newly developed NPC-SVM classifier based on tumor-associated biomarkers will facilitate patient counseling and individualize management of patients with NPC.

    View details for DOI 10.1200/JCO.2010.33.7741

    View details for Web of Science ID 000298136500018

    View details for PubMedID 22025164

  • Sunlight exposure, vitamin D, and risk of non-Hodgkin lymphoma in the Nurses' Health Study CANCER CAUSES & CONTROL Bertrand, K. A., Chang, E. T., Abel, G. A., Zhang, S. M., Spiegelman, D., Qureshi, A. A., Laden, F. 2011; 22 (12): 1731-1741

    Abstract

    Case-control studies suggest increased sun exposure reduces non-Hodgkin lymphoma (NHL) risk. Evidence from prospective cohort studies, however, is limited and inconsistent. We evaluated the association between ambient ultraviolet radiation (UV) exposure and NHL in a nationwide cohort of women, the Nurses' Health Study (NHS).Between 1976 and 2006, we identified 1064 incident NHL cases among 115,482 women in the prospective NHS. Exposures assessed included average annual UV-B flux based on residence at various times during life, vitamin D intake, and predicted plasma 25-hydroxyvitamin D levels. We estimated incidence rate ratios (RRs) and 95% confidence intervals (CIs) for risk of all NHL and histologic subtypes using Cox proportional hazards models.NHL risk was increased for women residing in areas of high ambient UV radiation (UV-B flux >113 R-B count × 10(-4)) compared to those with lower exposure (<113), with positive linear trends at all time points. The multivariable-adjusted RR for high UV area at age 15 was 1.21 (95% CI: 1.00, 1.47; p-trend < 0.01). There was no evidence of statistical heterogeneity by subtype, although power was limited for subtype analyses. We observed no association between vitamin D measures and risk of NHL overall or by subtype.Our findings do not support the hypothesis of a protective effect of UV radiation exposure on NHL risk. We found no association between vitamin D and NHL risk.

    View details for DOI 10.1007/s10552-011-9849-x

    View details for Web of Science ID 000297799200012

    View details for PubMedID 21987081

  • Long-Term Exposure to Air Pollution and Cardiorespiratory Disease in the California Teachers Study Cohort AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE Lipsett, M. J., Ostro, B. D., Reynolds, P., Goldberg, D., Hertz, A., Jerrett, M., Smith, D. F., Garcia, C., Chang, E. T., Bernstein, L. 2011; 184 (7): 828-835

    Abstract

    Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease.To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause specific mortality.We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals.We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models.We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 ?m in aerodynamic diameter (PM2.5), scaled to an increment of 10 ?g/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02-1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02-1.38). Long-term exposure to particulate matter less than 10 ?m in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99-1.14) and incident stroke (1.06; 95% CI, 1.00-1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality.This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

    View details for DOI 10.1164/rccm.201012-2082OC

    View details for Web of Science ID 000295407300017

    View details for PubMedID 21700913

  • Nutrients and Genetic Variation Involved in One-Carbon Metabolism and Hodgkin Lymphoma Risk: A Population-based Case-Control Study AMERICAN JOURNAL OF EPIDEMIOLOGY Kasperzyk, J. L., Chang, E. T., Birmann, B. M., Kraft, P., Zheng, T., Mueller, N. E. 2011; 174 (7): 816-827

    Abstract

    Nutritional and genetic determinants of the one-carbon metabolism pathway have been related to risk of malignant lymphomas, but little is known about their associations with Hodgkin lymphoma risk specifically. The authors examined nutrient intake (folate, vitamin B(2), vitamin B(6), vitamin B(12), methionine) and multivitamin use among 497 Hodgkin lymphoma patients and 638 population-based controls (Massachusetts and Connecticut, 1997-2000), and genetic variation (MTHFR 677C>T, MTHFR 1298A>C, MTR 2756A>G, SHMT1 1420C>T, TYMS 1494del6) and gene-diet interactions in a subset. Unconditional logistic regression was used to calculate multivariable odds ratios and 95% confidence intervals. Hodgkin lymphoma risk was not associated with total nutrient intake or intake from food alone (excluding supplements). Multivitamin use (odds ratio (OR) = 1.46, 95% CI: 1.09, 1.96), total vitamin B(6) (OR(quartile 4 vs. 1) = 1.62) (P(trend) = 0.03), and total vitamin B(12) (OR(quartile 4 vs. 1) = 1.75) (P(trend) = 0.02) intakes were positively associated with risk of Epstein-Barr virus-negative, but not -positive, disease. The 5 genetic variants were not significantly associated with Hodgkin lymphoma risk; no significant gene-diet interactions were observed after Bonferroni correction. Study findings do not support a strong role for nutrients and genetic variation in the one-carbon metabolism pathway in susceptibility to Hodgkin lymphoma. Associations between diet and risk of Epstein-Barr virus-negative disease require confirmation in other populations.

    View details for DOI 10.1093/aje/kwr190

    View details for Web of Science ID 000295166500008

    View details for PubMedID 21810727

  • Cigarette Smoking, Passive Smoking, and Non-Hodgkin Lymphoma Risk: Evidence From the California Teachers Study AMERICAN JOURNAL OF EPIDEMIOLOGY Lu, Y., Wang, S. S., Reynolds, P., Chang, E. T., Ma, H., Sullivan-Halley, J., Clarke, C. A., Bernstein, L. 2011; 174 (5): 563-573

    Abstract

    Epidemiologic studies conducted to date have shown evidence of a causal relation between smoking and non-Hodgkin lymphoma (NHL) risk. However, previous studies did not account for passive smoking exposure in the never-smoking reference group. The California Teachers Study collected information about lifetime smoking and household passive smoking exposure in 1995 and about lifetime exposure to passive smoking in 3 settings (household, workplace, and social settings) in 1997-1998. Multivariable-adjusted relative risks and 95% confidence intervals were estimated by fitting Cox proportional hazards models with follow-up through 2007. Compared with never smokers, ever smokers had a 1.11-fold (95% confidence interval (CI): 0.94, 1.30) higher NHL risk that increased to a 1.22-fold (95% CI: 0.95, 1.57) higher risk when women with household passive smoking were excluded from the reference category. Statistically significant dose responses were observed for lifetime cumulative smoking exposure (intensity and pack-years; both P 's for trend = 0.02) when women with household passive smoking were excluded from the reference category. Among never smokers, NHL risk increased with increasing lifetime exposure to passive smoking (relative risk = 1.51 (95% CI: 1.03, 2.22) for >40 years vs. ?5 years of passive smoking; P for trend = 0.03), particularly for follicular lymphoma (relative risk = 2.89 (95% CI: 1.23, 6.80); P for trend = 0.01). The present study provides evidence that smoking and passive smoking may influence NHL etiology, particularly for follicular lymphoma.

    View details for DOI 10.1093/aje/kwr127

    View details for Web of Science ID 000294356800009

    View details for PubMedID 21768403

  • Oral contraceptives, menopausal hormone therapy use and risk of B-cell non-Hodgkin lymphoma in the California Teachers Study INTERNATIONAL JOURNAL OF CANCER Lu, Y., Wang, S. S., Sullivan-Halley, J., Chang, E. T., Clarke, C. A., Henderson, K. D., Ma, H., Duan, L., Lacey, J. V., Deapen, D., Bernstein, L. 2011; 129 (4): 974-982

    Abstract

    We examined oral contraceptive (OC) and menopausal hormonal therapy (MHT) use in relation to risk of B-cell non-Hodgkin lymphoma (NHL). Women under age 85 years participating in the California Teachers Study with no history of hematopoietic cancer were followed from 1995 through 2007. A total of 516 of 114,131 women eligible for OC use analysis and 402 of 54,758 postmenopausal women eligible for MHT use analysis developed B-cell NHL. Multivariable adjusted and age stratified Cox proportional hazards models were fit to estimate relative risks (RRs) and 95% confidence intervals (95% CI). Ever versus never OC use was marginally associated with lower B-cell NHL risk, particularly among women first using OCs before age 25 years (RR=0.72, 95% CI=0.51-0.99); yet, no duration-response effect was observed. No association was observed for ever versus never MHT use among postmenopausal women (RR=1.05, 95% CI=0.83-1.33) overall or by formulation (estrogen alone, ET, or estrogen plus progestin, EPT). Among women with no MHT use, having bilateral oophorectomy plus hysterectomy was associated with greater B-cell NHL risk than having natural menopause (RR=3.15, 95% CI=1.62-6.13). Bilateral oophorectomy plus hysterectomy was not associated with risk among women who used ET or EPT. These results indicate that exogenous hormone use does not strongly influence B-cell NHL risk.

    View details for DOI 10.1002/ijc.25730

    View details for Web of Science ID 000292508000023

    View details for PubMedID 20957632

  • San Francisco Hep B Free: A Grassroots Community Coalition to Prevent Hepatitis B and Liver Cancer JOURNAL OF COMMUNITY HEALTH Bailey, M. B., Shiau, R., Zola, J., Fernyak, S. E., Fang, T., So, S. K., Chang, E. T. 2011; 36 (4): 538-551

    Abstract

    Chronic hepatitis B is the leading cause of liver cancer and the largest health disparity between Asian/Pacific Islanders (APIs) and the general US population. The Hep B Free model was launched to eliminate hepatitis B infection by increasing hepatitis B awareness, testing, vaccination, and treatment among APIs by building a broad, community-wide coalition. The San Francisco Hep B Free campaign is a diverse public/private collaboration unifying the API community, health care system, policy makers, businesses, and the general public in San Francisco, California. Mass-media and grassroots messaging raised citywide awareness of hepatitis B and promoted use of the existing health care system for hepatitis B screening and follow-up. Coalition partners reported semi-annually on activities, resources utilized, and system changes instituted. From 2007 to 2009, over 150 organizations contributed approximately $1,000,000 in resources to the San Francisco Hep B Free campaign. 40 educational events reached 1,100 healthcare providers, and 50% of primary care physicians pledged to screen APIs routinely for hepatitis B. Community events and fairs reached over 200,000 members of the general public. Of 3,315 API clients tested at stand-alone screening sites created by the campaign, 6.5% were found to be chronically infected and referred to follow-up care. A grassroots coalition that develops strong partnerships with diverse organizations can use existing resources to successfully increase public and healthcare provider awareness about hepatitis B among APIs, promote routine hepatitis B testing and vaccination as part of standard primary care, and ensure access to treatment for chronically infected individuals.

    View details for DOI 10.1007/s10900-010-9339-1

    View details for Web of Science ID 000292513300006

    View details for PubMedID 21125320

  • Asian ethnicity and breast cancer subtypes: a study from the California Cancer Registry BREAST CANCER RESEARCH AND TREATMENT Telli, M. L., Chang, E. T., Kurian, A. W., Keegan, T. H., McClure, L. A., Lichtensztajn, D., Ford, J. M., Gomez, S. L. 2011; 127 (2): 471-478

    Abstract

    The distribution of breast cancer molecular subtypes has been shown to vary by race/ethnicity, highlighting the importance of host factors in breast tumor biology. We undertook the current analysis to determine population-based distributions of breast cancer subtypes among six ethnic Asian groups in California. We defined immunohistochemical (IHC) surrogates for each breast cancer subtype among Chinese, Japanese, Filipina, Korean, Vietnamese, and South Asian patients diagnosed with incident, primary, invasive breast cancer between 2002 and 2007 in the California Cancer Registry as: hormone receptor-positive (HR+)/HER2- [estrogen receptor-positive (ER+) and/or progesterone receptor-positive (PR+), human epidermal growth factor receptor 2-negative (HER2-)], triple-negative (ER-, PR-, and HER2-), and HER2-positive (ER±, PR±, and HER2+). We calculated frequencies of breast cancer subtypes among Asian ethnic groups and evaluated their associations with clinical and demographic factors. Complete IHC data were available for 8,140 Asian women. Compared to non-Hispanic White women, Korean [odds ratio (OR) = 1.8, 95% confidence interval (CI) = 1.5-2.2], Filipina (OR = 1.3, 95% CI = 1.2-1.5), Vietnamese (OR = 1.3, 95% CI = 1.1-1.6), and Chinese (OR = 1.1, 95% CI = 1.0-1.3) women had a significantly increased risk of being diagnosed with HER2-positive breast cancer subtypes after adjusting for age, stage, grade, socioeconomic status, histology, diagnosis year, nativity, and hospital ownership status. We report a significant ethnic disparity in HER2-positive breast cancer in a large population-based cohort enriched for Asian-Americans. Given the poor prognosis and high treatment costs of HER2-positive breast cancer, our results have implications for healthcare resource utilization, cancer biology, and clinical care.

    View details for DOI 10.1007/s10549-010-1173-8

    View details for Web of Science ID 000290227900017

    View details for PubMedID 20957431

  • Lymphoid Malignancies in US Asians: Incidence Rate Differences by Birthplace and Acculturation CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Clarke, C. A., Glaser, S. L., Gomez, S. L., Wang, S. S., Keegan, T. H., Yang, J., Chang, E. T. 2011; 20 (6): 1064-1077

    Abstract

    Malignancies of the lymphoid cells, including non-Hodgkin lymphomas (NHL), HL, and multiple myeloma, occur at much lower rates in Asians than other racial/ethnic groups in the United States. It remains unclear whether these deficits are explained by genetic or environmental factors. To better understand environmental contributions, we examined incidence patterns of lymphoid malignancies among populations characterized by ethnicity, birthplace, and residential neighborhood socioeconomic status (SES) and ethnic enclave status.We obtained data about all Asian patients diagnosed with lymphoid malignancies between 1988 and 2004 from the California Cancer Registry and neighborhood characteristics from U.S. Census data.Although incidence rates of most lymphoid malignancies were lower among Asian than white populations, only follicular lymphoma (FL), chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), and nodular sclerosis (NS) HL rates were statistically significantly lower among foreign-born than U.S.-born Asians with incidence rate ratios ranging from 0.34 to 0.87. Rates of CLL/SLL and NS HL were also lower among Asian women living in ethnic enclaves or lower SES neighborhoods than those living elsewhere.These observations support strong roles of environmental factors in the causation of FL, CLL/SLL, and NS HL.Studying specific lymphoid malignancies in U.S. Asians may provide valuable insight toward understanding their environmental causes.

    View details for DOI 10.1158/1055-9965.EPI-11-0038

    View details for Web of Science ID 000291308600003

    View details for PubMedID 21493873

  • Head and Neck Cancer-Specific Survival Based on Socioeconomic Status in Asians and Pacific Islanders CANCER Chu, K. P., Shema, S., Wu, S., Gomez, S. L., Chang, E. T., Quynh-Thu Le, Q. T. 2011; 117 (9): 1935-1945

    Abstract

    Lower socioeconomic status (SES) has been linked to higher incidence of head and neck cancer (HNC) and lower survival. However, little is known about the effect of SES on HNC survival in Asians and Pacific Islanders (APIs). This study's purpose was to examine the effect of SES on disease-specific survival (DSS) and overall survival (OS) in APIs with HNC using population-based data.A total of 53,544 HNC patients (4,711 = APIs) were identified from the California Cancer Registry from 1988 to 2007. Neighborhood (block-group-level) SES, based on composite Census 1990 and 2000 data, was calculated for each patient based on address at diagnosis, categorized into statewide quintiles, and collapsed into 2 groups for comparison (low SES = quintiles 1-3; high SES = quintiles 4-5). DSS and OS were computed by the Kaplan-Meier method. Adjusted hazards ratios (HR) were estimated using Cox proportional hazards regression models.Among APIs, lower neighborhood SES was significantly associated with poorer DSS (HR range for oral cavity, oropharynx, or larynx/hypopharynx cancer, 1.07-1.34) and OS (HR, 1.13-1.37) after adjusting for patient and tumor characteristics. Lower SES was significantly associated with poorer survival in API with all HNC sites combined: DSS HR: 1.26 (95% confidence interval [CI], 1.08-1.48) and OS HR, 1.30 (95% CI, 1.16-1.45).Neighborhood SES was associated with longer DSS and OS in API with HNC. The effect of SES on HNC survival should be considered in future studies, and particular attention should be paid to clinical care of lower-SES HNC patients.

    View details for DOI 10.1002/cncr.25723

    View details for Web of Science ID 000289833100020

    View details for PubMedID 21509771

  • GWAS of Follicular Lymphoma Reveals Allelic Heterogeneity at 6p21.32 and Suggests Shared Genetic Susceptibility with Diffuse Large B-cell Lymphoma PLOS GENETICS Smedby, K. E., Foo, J. N., Skibola, C. F., Darabi, H., Conde, L., Hjalgrim, H., Kumar, V., Chang, E. T., Rothman, N., Cerhan, J. R., Brooks-Wilson, A. R., Rehnberg, E., Irwan, I. D., Ryder, L. P., Brown, P. N., Bracci, P. M., Agana, L., Riby, J., Cozen, W., Davis, S., Hartge, P., Morton, L. M., Severson, R. K., Wang, S. S., Slager, S. L., Fredericksen, Z. S., Novak, A. J., Kay, N. E., Habermann, T. M., Armstrong, B., Kricker, A., Milliken, S., Purdue, M. P., Vajdic, C. M., Boyle, P., Lan, Q., Zahm, S. H., Zhang, Y., Zheng, T., Leach, S., Spinelli, J. J., Smith, M. T., Chanock, S. J., Padyukov, L., Alfredsson, L., Klareskog, L., Glimelius, B., Melbye, M., Liu, E. T., Adami, H., Humphreys, K., Liu, J. 2011; 7 (4)

    Abstract

    Non-Hodgkin lymphoma (NHL) represents a diverse group of hematological malignancies, of which follicular lymphoma (FL) is a prevalent subtype. A previous genome-wide association study has established a marker, rs10484561 in the human leukocyte antigen (HLA) class II region on 6p21.32 associated with increased FL risk. Here, in a three-stage genome-wide association study, starting with a genome-wide scan of 379 FL cases and 791 controls followed by validation in 1,049 cases and 5,790 controls, we identified a second independent FL-associated locus on 6p21.32, rs2647012 (OR(combined)? = 0.64, P(combined)? = 2 × 10(-21)) located 962 bp away from rs10484561 (r(2)<0.1 in controls). After mutual adjustment, the associations at the two SNPs remained genome-wide significant (rs2647012:OR(adjusted) ?= 0.70, P(adjusted)? =? 4 × 10(-12); rs10484561:OR(adjusted) ?= 1.64, P(adjusted) ?= 5 × 10(-15)). Haplotype and coalescence analyses indicated that rs2647012 arose on an evolutionarily distinct haplotype from that of rs10484561 and tags a novel allele with an opposite (protective) effect on FL risk. Moreover, in a follow-up analysis of the top 6 FL-associated SNPs in 4,449 cases of other NHL subtypes, rs10484561 was associated with risk of diffuse large B-cell lymphoma (OR(combined) ?= 1.36, P(combined)? =? 1.4 × 10(-7)). Our results reveal the presence of allelic heterogeneity within the HLA class II region influencing FL susceptibility and indicate a possible shared genetic etiology with diffuse large B-cell lymphoma. These findings suggest that the HLA class II region plays a complex yet important role in NHL.

    View details for DOI 10.1371/journal.pgen.1001378

    View details for Web of Science ID 000289977000026

    View details for PubMedID 21533074

  • Papillary thyroid cancer incidence rates vary significantly by birthplace in Asian American women CANCER CAUSES & CONTROL Horn-Ross, P. L., McClure, L. A., Chang, E. T., Clarke, C. A., Keegan, T. H., Rull, R. P., Quach, T., Gomez, S. L. 2011; 22 (3): 479-485

    Abstract

    To investigate how birthplace influences the incidence of papillary thyroid cancer among Asian American women.Birthplace- and ethnic-specific age-adjusted and age-specific incidence rates were calculated using data from the California Cancer Registry for the period 1988-2004. Birthplace was statistically imputed for 30% of cases using a validated imputation method based on age at Social Security number issuance. Population estimates were obtained from the US Census. Incidence rate ratios (IRR) and 95% confidence intervals (CI) were estimated for foreign-born vs. US-born women.Age-adjusted incidence rates of papillary thyroid cancer among Filipina (13.7 per 100,000) and Vietnamese (12.7) women were more than double those of Japanese women (6.2). US-born Chinese (IRR = 0.48, 95% CI: 0.40-0.59) and Filipina women (IRR = 0.74, 95% CI: 0.58-0.96) had significantly higher rates than those who were foreign-born; the opposite was observed for Japanese women (IRR = 1.55, 95% CI: 1.17-2.08). The age-specific patterns among all foreign-born Asian women and US-born Japanese women showed a slow steady increase in incidence until age 70. However, among US-born Asian women (except Japanese), substantially elevated incidence rates during the reproductive and menopausal years were evident.Ethnic- and birthplace-variation in papillary thyroid cancer incidence can provide insight into the etiology of this increasingly common and understudied cancer.

    View details for DOI 10.1007/s10552-010-9720-5

    View details for Web of Science ID 000288542400015

    View details for PubMedID 21207130

  • Survival following Non-Small Cell Lung Cancer among Asian/Pacific Islander, Latina, and Non-Hispanic White Women Who Have Never Smoked CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Gomez, S. L., Chang, E. T., Shema, S. J., Fish, K., Sison, J. D., Reynolds, P., Clement-Duchene, C., Wrensch, M. R., Wiencke, J. L., Wakelee, H. A. 2011; 20 (3): 545-554

    Abstract

    Lung cancer is the leading cause of cancer death among U.S. Asian/Pacific Islander (API) and Latina women despite low smoking prevalence. This study examined survival patterns following non-small cell lung cancer in a population-based sample of lung cancer cases from the San Francisco Bay Area Lung Cancer Study (SFBALCS).Women diagnosed with lung cancer from 1998 to 2003 and 2005 to 2008 and identified through the Greater Bay Area Cancer Registry were telephone-screened for eligibility for the SFBALCS. The screener data were linked to the cancer registry data to determine follow-up. This analysis included 187 non-Hispanic (NH) white, 23 U.S.-born Latina, 32 foreign-born Latina, 30 U.S.-born API, and 190 foreign-born API never-smokers diagnosed with lung cancer and followed through 2008.All-cause survival was poorer among APIs [HR=1.7 (95% CI: 1.0-2.8) among U.S.-born APIs and HR=1.2 (95% CI: 0.9-1.5) among foreign-born APIs] and Latinas [HR=2.1 (95% CI: 1.2-3.6) among U.S.-born Latinas; HR=1.4 (95% CI: 0.9-2.3) among foreign-born Latinas] relative to NH whites. These survival differences were not explained by differences in selected sociodemographic or clinical factors.Further research should focus on factors such as cultural behaviors, access to or attitudes toward health care, and genetic variations as possible explanations for these striking racial/ethnic differences.Latina and API female never-smokers diagnosed with lung cancer were up to two times more likely to die than NH whites, highlighting the need for additional research to identify the underlying reasons for the disparities and heightened clinical awareness.

    View details for DOI 10.1158/1055-9965.EPI-10-0965

    View details for Web of Science ID 000288067200017

    View details for PubMedID 21239685

  • Age-specific effects of hormone therapy use on overall mortality and ischemic heart disease mortality among women in the California Teachers Study MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY Stram, D. O., Liu, Y., Henderson, K. D., Sullivan-Halley, J., Luo, J., Saxena, T., Reynolds, P., Chang, E. T., Neuhausen, S. L., Horn-Ross, P. L., Bernstein, L., Ursin, G. 2011; 18 (3): 253-261

    Abstract

    Although the Women's Health Initiative trial suggested that menopausal hormone therapy (HT) does not reduce coronary heart disease mortality overall, subsequent results have suggested that there may be a benefit in younger women. The California Teachers Study questionnaire and mortality data were used to examine whether age modified the association between HT and the relative risk of overall mortality and ischemic heart disease deaths.Participants from the California Teachers Study were 71,237 postmenopausal women (mean age, 63 y; range, 36-94 y) followed prospectively for mortality and other outcomes from 1995-1996 through 2004.Age at baseline was a much more important modifier of HT effects than was age at start of therapy. Risks for all-cause mortality (n = 8,399) were lower for younger current HT users at baseline than for never users (for women ? 0 y: hazard ratio, 0.54; 95% CI, 0.46-0.62). These risk reductions greatly diminished, in a roughly linear fashion, with increasing baseline age (for women 85-94 y: hazard ratio, 0.94; 95% CI, 0.81-1.10 for all-cause mortality). Similar results were seen for ischemic heart disease deaths (n = 1,464). No additional significant modifying effects of age at first use, duration of use, or formulation were apparent.These results provide evidence that reduced risks of mortality associated with HT use are observed among younger users but not for older postmenopausal women, even those starting therapy close to their time of menopause.

    View details for DOI 10.1097/gme.0b013e3181f0839a

    View details for Web of Science ID 000287658600006

    View details for PubMedID 20881652

  • A genome-wide association study of Hodgkin's lymphoma identifies new susceptibility loci at 2p16.1 (REL), 8q24.21 and 10p14 (GATA3) NATURE GENETICS Enciso-Mora, V., Broderick, P., Ma, Y., Jarrett, R. F., Hjalgrim, H., Hemminki, K., van den Berg, A., Olver, B., Lloyd, A., Dobbins, S. E., Lightfoot, T., van Leeuwen, F. E., Foersti, A., Diepstra, A., Broeks, A., Vijayakrishnan, J., Shield, L., Lake, A., Montgomery, D., Roman, E., Engert, A., von Strandmann, E. P., Reiners, K. S., Nolte, I. M., Smedby, K. E., Adami, H., Russell, N. S., Glimelius, B., Hamilton-Dutoit, S., de Bruin, M., Ryder, L. P., Molin, D., Sorensen, K. M., Chang, E. T., Taylor, M., Cooke, R., Hofstra, R., Westers, H., van Wezel, T., van Eijk, R., Ashworth, A., Rostgaard, K., Melbye, M., Swerdlow, A. J., Houlston, R. S. 2010; 42 (12): 1126-?

    Abstract

    To identify susceptibility loci for classical Hodgkin's lymphoma (cHL), we conducted a genome-wide association study of 589 individuals with cHL (cases) and 5,199 controls with validation in four independent samples totaling 2,057 cases and 3,416 controls. We identified three new susceptibility loci at 2p16.1 (rs1432295, REL, odds ratio (OR) = 1.22, combined P = 1.91 × 10(-8)), 8q24.21 (rs2019960, PVT1, OR = 1.33, combined P = 1.26 × 10(-13)) and 10p14 (rs501764, GATA3, OR = 1.25, combined P = 7.05 × 10(-8)). Furthermore, we confirmed the role of the major histocompatibility complex in disease etiology by revealing a strong human leukocyte antigen (HLA) association (rs6903608, OR = 1.70, combined P = 2.84 × 10(-50)). These data provide new insight into the pathogenesis of cHL.

    View details for DOI 10.1038/ng.696

    View details for Web of Science ID 000284578800017

    View details for PubMedID 21037568

  • Body size and the risk of ovarian cancer by hormone therapy use in the California Teachers Study cohort CANCER CAUSES & CONTROL Canchola, A. J., Chang, E. T., Bernstein, L., Largent, J. A., Reynolds, P., Deapen, D., Henderson, K. D., Ursin, G., Horn-Ross, P. L. 2010; 21 (12): 2241-2248

    Abstract

    To investigate whether obesity and hormone therapy (HT) are associated with ovarian cancer risk among women in the California Teachers Study cohort.Of 56,091 women age ? 45 years, 277 developed epithelial ovarian cancer between 1995 and 2007. Multivariate Cox regression was performed.Among women who never used HT, greater adult weight gain, waist circumference and waist-to-height ratio, but not adult BMI, increased risk of ovarian cancer. Compared to women who never used HT and had a stable adult weight, risk of ovarian cancer was increased in women who gained ? 40 lb (relative risk (RR) 1.8, 95% confidence interval (CI): 1.0-3.0) or used HT for >5 years (RR 2.3 95% CI: 1.3-4.1). Having both exposures (RR 1.9, 95% CI: 0.99-3.5), however, did not increase risk more than having either alone. Results were similar for waist circumference and weight-to-height ratio; however, differences across HT groups were not statistically significant.This study suggests that abdominal adiposity and weight gain, but not overall obesity, increase ovarian cancer risk and that there may be a threshold level beyond which additional hormones, whether exogenous or endogenous, do not result in additional elevation in risk. However, large pooled analyses are needed to confirm these findings.

    View details for DOI 10.1007/s10552-010-9647-x

    View details for Web of Science ID 000288609600032

    View details for PubMedID 20924664

  • A prospective study of Epstein-Barr virus antibodies and risk of non-Hodgkin lymphoma BLOOD Bertrand, K. A., Birmann, B. M., Chang, E. T., Spiegelman, D., Aster, J. C., Zhang, S. M., Laden, F. 2010; 116 (18): 3547-3553

    Abstract

    Severe immunosuppression is an established risk factor for non-Hodgkin lymphoma (NHL), but an association with subclinical immune dysfunction is unclear. We conducted a case-control study nested in the Physicians' Health Study and the Nurses' Health Study cohorts to determine whether patterns of antibody response to Epstein-Barr virus (EBV) were associated with NHL risk. We measured antibody titers against viral capsid antigen, early antigen, and Epstein-Barr nuclear antigen (EBNA-1 and EBNA-2) in blood samples collected before diagnosis from 340 cases and 662 matched controls. Using conditional logistic regression, we estimated rate ratios (RRs) and 95% confidence intervals (CIs) for elevated versus normal titers and the ratio of anti-EBNA-1 to anti-EBNA-2 titers (? 1.0 vs > 1.0). We found no association between EBV serostatus, elevated titers, or an EBNA-1/EBNA-2 ratio ? 1.0 and NHL risk overall. For chronic lymphocytic leukemia/small lymphocytic lymphoma, suggestive associations were noted for elevated anti-EBNA-2 (RR, 1.74; 95% CI, 0.99-3.05), anti-viral capsid antigen (RR, 1.58; 95% CI, 0.79-3.14), and EBNA-1/EBNA-2 ratio ? 1.0 (RR, 1.52; 95% CI, 0.91-2.55). There was no evidence of heterogeneity by subtype. Overall, we found no evidence that EBV antibody profile predicts NHL risk in immunocompetent persons, with the possible exception of chronic lymphocytic leukemia/small lymphocytic lymphoma.

    View details for DOI 10.1182/blood-2010-05-282715

    View details for Web of Science ID 000283853200024

    View details for PubMedID 20647565

  • HIGHER INCIDENCE OF HEAD AND NECK CANCERS AMONG VIETNAMESE AMERICAN MEN IN CALIFORNIA HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK Filion, E. J., McClure, L. A., Huang, D., Seng, K., Kaplan, M. J., Colevas, A. D., Gomez, S. L., Chang, E. T., Le, Q. 2010; 32 (10): 1336-1344

    Abstract

    Our aim was to determine the incidence rates of head and neck cancer in Vietnamese Californians compared with other Asian and non-Asian Californians.Age-adjusted incidence rates of head and neck cancer between 1988 and 2004 were computed for Vietnamese Californians compared with other racial/ethnic groups by time period, ethnicity, neighborhood-level socioeconomic status (SES), and sex using data from the population-based California Cancer Registry (CCR). Data by smoking and alcohol status were tabulated from the California Health Interview Survey.Vietnamese men had a higher incidence rate of head and neck cancer than other Asian men. Specifically, the laryngeal cancer rate was significantly higher for Vietnamese men (6.5/100,000; 95% confidence interval [CI], 5.0-8.2) than all other Asian men (range, 2.6-3.8/100,000), except Korean men (5.1/100,000; 95% CI, 3.9-6.4). Both Vietnamese and Korean men had the highest percentage of current smokers. Neighborhood SES was inversely related to head and neck cancer rates among Vietnamese men and women.The higher incidence rate of head and neck cancer in Vietnamese men may correspond to the higher smoking prevalence in this group. Individual-level data are needed to establish the link of tobacco, alcohol, and other risk factors with head and neck cancer in these patients.

    View details for DOI 10.1002/hed.21330

    View details for Web of Science ID 000282707500008

    View details for PubMedID 20091688

  • Past recreational physical activity, body size, and all-cause mortality following breast cancer diagnosis: results from the breast cancer family registry BREAST CANCER RESEARCH AND TREATMENT Keegan, T. H., Milne, R. L., Andrulis, I. L., Chang, E. T., Sangaramoorthy, M., Phillips, K., Giles, G. G., Goodwin, P. J., Apicella, C., Hopper, J. L., Whittemore, A. S., John, E. M. 2010; 123 (2): 531-542

    Abstract

    Few studies have considered the joint association of body mass index (BMI) and physical activity, two modifiable factors, with all-cause mortality after breast cancer diagnosis. Women diagnosed with invasive breast cancer (n = 4,153) between 1991 and 2000 were enrolled in the Breast Cancer Family Registry through population-based sampling in Northern California, USA; Ontario, Canada; and Melbourne and Sydney, Australia. During a median follow-up of 7.8 years, 725 deaths occurred. Baseline questionnaires assessed moderate and vigorous recreational physical activity and BMI prior to diagnosis. Associations with all-cause mortality were assessed using Cox proportional hazards regression, adjusting for established prognostic factors. Compared with no physical activity, any recreational activity during the 3 years prior to diagnosis was associated with a 34% lower risk of death [hazard ratio (HR) = 0.66, 95% confidence interval (CI): 0.51-0.85] for women with estrogen receptor (ER)-positive tumors, but not those with ER-negative tumors; this association did not appear to differ by race/ethnicity or BMI. Lifetime physical activity was not associated with all-cause mortality. BMI was positively associated with all-cause mortality for women diagnosed at age > or =50 years with ER-positive tumors (compared with normal-weight women, HR for overweight = 1.39, 95% CI: 0.90-2.15; HR for obese = 1.77, 95% CI: 1.11-2.82). BMI associations did not appear to differ by race/ethnicity. Our findings suggest that physical activity and BMI exert independent effects on overall mortality after breast cancer.

    View details for DOI 10.1007/s10549-010-0774-6

    View details for Web of Science ID 000280807900023

    View details for PubMedID 20140702

  • Body size and the risk of endometrial cancer by hormone therapy use in postmenopausal women in the California Teachers Study cohort CANCER CAUSES & CONTROL Canchola, A. J., Chang, E. T., Bernstein, L., Largent, J. A., Reynolds, P., Deapen, D., Ursin, G., Horn-Ross, P. L. 2010; 21 (9): 1407-1416

    Abstract

    To investigate whether hormone therapy (HT) and obesity are associated with endometrial cancer risk among postmenopausal women in the California Teachers Study cohort.Of 28,418 postmenopausal women, 395 developed type 1 endometrial cancer between 1995 and 2006. Multivariate Cox regression was performed to estimate relative risks (RR), stratified by HT use (never used, ever estrogen alone (ET) or exclusively estrogen-plus-progestin (EPT)).Among women who never used HT, overall and abdominal adiposity were associated with increased risk; when evaluated simultaneously, abdominal adiposity was more strongly associated (RR 2.2, 95% confidence interval (CI): 1.1-4.5 for waist >or=35 vs. <35 inches). Among women who ever used ET, risk was increased in women with BMI >or= 25 kg/m(2) (RR 1.6, 95% CI: 1.1-2.3 vs. <25 kg/m(2)). Neither overall nor abdominal obesity was associated with risk in women who exclusively used EPT (p-interaction <0.001 for BMI by HT use).Among women who never used HT, risk was strongly positively related to obesity and may have been influenced more by abdominal than by overall adiposity; however, due to small numbers, this latter finding requires replication. Among women who ever used ET, being overweight at baseline predicted higher risk, whereas use of EPT mitigated any effects of obesity.

    View details for DOI 10.1007/s10552-010-9568-8

    View details for Web of Science ID 000280902000006

    View details for PubMedID 20431936

  • Genome-wide association study of follicular lymphoma identifies a risk locus at 6p21.32 NATURE GENETICS Conde, L., Halperin, E., Akers, N. K., Brown, K. M., Smedby, K. E., Rothman, N., Nieters, A., Slager, S. L., Brooks-Wilson, A., Agana, L., Riby, J., Liu, J., Adami, H., Darabi, H., Hjalgrim, H., Low, H., Humphreys, K., Melbye, M., Chang, E. T., Glimelius, B., Cozen, W., Davis, S., Hartge, P., Morton, L. M., Schenk, M., Wang, S. S., Armstrong, B., Kricker, A., Milliken, S., Purdue, M. P., Vajdic, C. M., Boyle, P., Lan, Q., Zahm, S. H., Zhang, Y., Zheng, T., Becker, N., Benavente, Y., Boffetta, P., Brennan, P., Butterbach, K., Cocco, P., Foretova, L., Maynadie, M., de Sanjose, S., Staines, A., Spinelli, J. J., Achenbach, S. J., Call, T. G., Camp, N. J., Glenn, M., Caporaso, N. E., Cerhan, J. R., Cunningham, J. M., Goldin, L. R., Hanson, C. A., Kay, N. E., Lanasa, M. C., Leis, J. F., Marti, G. E., Rabe, K. G., Rassenti, L. Z., Spector, L. G., Strom, S. S., Vachon, C. M., Weinberg, J. B., Holly, E. A., Chanock, S., Smith, M. T., Bracci, P. M., Skibola, C. F. 2010; 42 (8): 661-664

    Abstract

    To identify susceptibility loci for non-Hodgkin lymphoma subtypes, we conducted a three-stage genome-wide association study. We identified two variants associated with follicular lymphoma at 6p21.32 (rs10484561, combined P = 1.12 x 10(-29) and rs7755224, combined P = 2.00 x 10(-19); r(2) = 1.0), supporting the idea that major histocompatibility complex genetic variation influences follicular lymphoma susceptibility. We also found confirmatory evidence of a previously reported association between chronic lymphocytic leukemia/small lymphocytic lymphoma and rs735665 (combined P = 4.24 x 10(-9)).

    View details for DOI 10.1038/ng.626

    View details for Web of Science ID 000280524000008

    View details for PubMedID 20639881

  • Parents' Ages at Birth and Risk of Adult-onset Hematologic Malignancies Among Female Teachers in California AMERICAN JOURNAL OF EPIDEMIOLOGY Lu, Y., Ma, H., Sullivan-Halley, J., Henderson, K. D., Chang, E. T., Clarke, C. A., Neuhausen, S. L., West, D. W., Bernstein, L., Wang, S. S. 2010; 171 (12): 1262-1269

    Abstract

    Although advanced parental age at one's birth has been associated with increased risk of breast and prostate cancers, few studies have examined its effect on adult-onset sporadic hematologic malignancies. The authors examined the association of parents' ages at women's births with risk of hematologic malignancies among 110,999 eligible women aged 22-84 years recruited into the prospective California Teachers Study. Between 1995 and 2007, 819 women without a family history of hematologic malignancies were diagnosed with incident lymphoma, leukemia (primarily acute myeloid leukemia), or multiple myeloma. Multivariable-adjusted Cox proportional hazards models provided estimates of relative risks and 95% confidence intervals. Paternal age was positively associated with non-Hodgkin lymphoma after adjustment for race and birth order (relative risk for age > or =40 vs. <25 years = 1.51, 95% confidence interval: 1.08, 2.13; P-trend = 0.01). Further adjustment for maternal age did not materially alter the association. By contrast, the elevated non-Hodgkin lymphoma risk associated with advanced maternal age (> or =40 years) became null when paternal age was included in the statistical model. No association was observed for acute myeloid leukemia or multiple myeloma. Advanced paternal age may play a role in non-Hodgkin lymphoma etiology. Potential etiologic mechanisms include de novo gene mutations, aberrant paternal gene imprinting, or telomere/telomerase biology.

    View details for DOI 10.1093/aje/kwq090

    View details for Web of Science ID 000278435700002

    View details for PubMedID 20507900

  • Racial and social class gradients in life expectancy in contemporary California SOCIAL SCIENCE & MEDICINE Clarke, C. A., Miller, T., Chang, E. T., Yin, D., Cockburn, M., Gomez, S. L. 2010; 70 (9): 1373-1380

    Abstract

    Life expectancy, or the estimated average age of death, is among the most basic measures of a population's health. However, monitoring differences in life expectancy among sociodemographically defined populations has been challenging, at least in the United States (US), because death certification does not include collection of markers of socioeconomic status (SES). In order to understand how SES and race/ethnicity independently and jointly affected overall health in a contemporary US population, we assigned a small-area-based measure of SES to all 689,036 deaths occurring in California during a three-year period (1999-2001) overlapping the most recent US census. Residence at death was geocoded to the smallest census area available (block group) and assigned to a quintile of a multifactorial SES index. We constructed life tables using mortality rates calculated by age, sex, race/ethnicity and neighborhood SES quintile, and produced corresponding life expectancy estimates. We found a 19.6 (+/-0.6) year gap in life expectancy between the sociodemographic groups with the longest life expectancy (highest SES quintile of Asian females; 84.9 years) and the shortest (lowest SES quintile of African-American males; 65.3 years). A positive SES gradient in life expectancy was observed among whites and African-Americans but not Hispanics or Asians. Age-specific mortality disparities varied among groups. Race/ethnicity and neighborhood SES had substantial and independent influences on life expectancy, underscoring the importance of monitoring health outcomes simultaneously by these factors. African-American males living in the poorest 20% of California neighborhoods had life expectancy comparable to that reported for males living in developing countries. Neighborhood SES represents a readily-available metric for ongoing surveillance of health disparities in the US.

    View details for DOI 10.1016/j.socscimed.2010.01.003

    View details for Web of Science ID 000277500400016

    View details for PubMedID 20171001

  • Disparities in Breast Cancer Survival Among Asian Women by Ethnicity and Immigrant Status: A Population-Based Study AMERICAN JOURNAL OF PUBLIC HEALTH Gomez, S. L., Clarke, C. A., Shema, S. J., Chang, E. T., Keegan, T. H., Glaser, S. L. 2010; 100 (5): 861-869

    Abstract

    We investigated heterogeneity in ethnic composition and immigrant status among US Asians as an explanation for disparities in breast cancer survival.We enhanced data from the California Cancer Registry and the Surveillance, Epidemiology, and End Results program through linkage and imputation to examine the effect of immigrant status, neighborhood socioeconomic status, and ethnic enclave on mortality among Chinese, Japanese, Filipino, Korean, South Asian, and Vietnamese women diagnosed with breast cancer from 1988 to 2005 and followed through 2007.US-born women had similar mortality rates in all Asian ethnic groups except the Vietnamese, who had lower mortality risk (hazard ratio [HR] = 0.3; 95% confidence interval [CI] = 0.1, 0.9). Except for Japanese women, all foreign-born women had higher mortality than did US-born Japanese, the reference group. HRs ranged from 1.4 (95% CI = 1.2, 1.7) among Koreans to 1.8 (95% CI = 1.5, 2.2) among South Asians and Vietnamese. Little of this variation was explained by differences in disease characteristics.Survival after breast cancer is poorer among foreign- than US-born Asians. Research on underlying factors is needed, along with increased awareness and targeted cancer control.

    View details for DOI 10.2105/AJPH.2009.176651

    View details for Web of Science ID 000276828800021

    View details for PubMedID 20299648

  • Genetic variation in chromosomal translocation breakpoint and immune function genes and risk of non-Hodgkin lymphoma CANCER CAUSES & CONTROL Fernberg, P., Chang, E. T., Duvefelt, K., Hjalgrim, H., Eloranta, S., Sorensen, K. M., Porwit, A., Humphreys, K., Melbye, M., Smedby, K. E. 2010; 21 (5): 759-769

    Abstract

    Tumor necrosis factor (TNF) and interleukin 10 (IL10) are promising candidate susceptibility genes for non-Hodgkin lymphoma (NHL). Chromosomal translocation breakpoint genes are of interest, given their documented involvement in lymphoma progression.We analyzed 11 polymorphisms in BCL2, CCND1, MYC, TNF, and IL10 in a large, population-based, Danish-Swedish case-control study including 2,449 NHL cases and 1,980 controls. Relative risk of NHL was computed as odds ratios (OR).There was no clear evidence of associations between variants in BCL2, CCND1, and MYC and risk of NHL overall or subtypes. TNF rs1800629 was associated with risk of NHL (OR 1.53, 95% confidence interval, CI, 1.06-2.19 for minor allele homozygosity), T-cell lymphoma (OR 2.54, CI 1.27-5.09) and mantle cell lymphoma (OR 2.84, CI 1.38-5.87). IL10 rs1800890 was associated with risk of diffuse large B-cell lymphoma (OR 1.41, CI 1.08-1.85 for minor allele homozygosity) and mantle cell lymphoma (OR 1.77, CI 1.04-3.00). We did not replicate a previously reported interaction with autoimmunity.We found no support for a role of the studied variants in BCL2, CCND1, or MYC in risk of NHL or subtypes, but we provide further evidence of putative susceptibility loci in TNF and IL10 for specific NHL subtypes.

    View details for DOI 10.1007/s10552-010-9504-y

    View details for Web of Science ID 000276768500012

    View details for PubMedID 20087644

  • HLA-A alleles and infectious mononucleosis suggest a critical role for cytotoxic T-cell response in EBV-related Hodgkin lymphoma PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Hjalgrim, H., Rostgaard, K., Johnson, P. C., Lake, A., Shield, L., Little, A., Ekstrom-Smedby, K., Adami, H., Glimelius, B., Hamilton-Dutoit, S., Kane, E., Taylor, G. M., McConnachie, A., Ryder, L. P., Sundstrom, C., Andersen, P. S., Chang, E. T., Alexander, F. E., Melbye, M., Jarrett, R. F. 2010; 107 (14): 6400-6405

    Abstract

    A proportion of classical Hodgkin lymphoma (HL) is believed to be causally related to infection with the ubiquitous lymphotropic EBV. The determining factors for development of EBV-related HL remain poorly understood, but likely involve immunological control of the viral infection. Accordingly, markers of the HLA class I region have been associated with risk of EBV-related HL. To study the host genetic component of EBV-related HL further, we investigated the lymphoma's association with HLA-A*01 and HLA-A*02 simultaneously in the setting of infectious mononucleosis (IM), a risk factor for EBV-related HL, in a case-series analysis including 278 EBV-related and 656 EBV-unrelated cases of HL. By logistic regression, HLA-A*01 alleles [odds ratio (OR) per allele, 2.15; 95% CI, 1.60-2.88] were associated with increased and HLA-A*02 alleles (OR per allele, 0.70; 95% CI, 0.51-0.97) with decreased risk of EBV-related HL. These allele-specific associations corresponded to nearly 10-fold variation in risk of EBV-related HL between HLA-A*01 and HLA-A*02 homozygotes. History of IM was also associated with risk of EBV-related HL (OR, 3.40; 95% CI, 1.74-6.66). The association between history of IM and EBV-related HL was not seen in the presence of HLA-A*02 because this allele appeared to neutralize the effect of IM on EBV-related HL risk. Our findings suggest that HLA class I-restricted EBV-specific cytotoxic T-cell responses and events in the early immune response to EBV infection in IM play critical roles in the pathogenesis of EBV-related HL.

    View details for DOI 10.1073/pnas.0915054107

    View details for Web of Science ID 000276374400050

    View details for PubMedID 20308568

  • Increasing Mastectomy Rates for Early-Stage Breast Cancer? Population-Based Trends From California JOURNAL OF CLINICAL ONCOLOGY Gomez, S. L., Lichtensztajn, D., Kurian, A. W., Telli, M. L., Chang, E. T., Keegan, T. H., Glaser, S. L., Clarke, C. A. 2010; 28 (10): E155-E157

    View details for DOI 10.1200/JCO.2009.26.1032

    View details for Web of Science ID 000276152200036

    View details for PubMedID 20159812

  • Hepatitis B and liver cancer knowledge and practices among healthcare and public health professionals in China: a cross-sectional study BMC PUBLIC HEALTH Chao, J., Chang, E. T., So, S. K. 2010; 10

    Abstract

    Chronic hepatitis B virus (HBV) infection is the leading cause of liver disease and liver cancer and a major source of health-related discrimination in China. To better target HBV detection and prevention programs, it is necessary to assess existing HBV knowledge, educational resources, reporting, and preventive practices, particularly among those health professionals who would be responsible for implementing such programs.At the China National Conference on the Prevention and Control of Viral Hepatitis on April 26-29, 2004, the Asian Liver Center at Stanford University partnered with the China Foundation for Hepatitis Prevention and Control to distribute a voluntary written questionnaire to Chinese healthcare and public health professionals from regional and provincial Chinese Centers for Disease Control and Prevention, health departments, and medical centers. Correct responses to survey questions were summed into a total knowledge score, and multivariate linear regression was used to compare differences in the score by participant characteristics.Although the median score was 81% correct, knowledge about HBV was inadequate, even among such highly trained health professionals. Of the 250 participants who completed the survey, 34% did not know that chronic HBV infection is often asymptomatic and 29% did not know that chronic HBV infection confers a high risk of cirrhosis, liver cancer, and premature death. Furthermore, 34% failed to recognize all the modes of HBV transmission and 30% did not know the importance of the hepatitis B vaccine in preventing liver disease. Respondents who reported poorer preventive practices, such as not having personally been tested for HBV and not routinely disposing of used medical needles, scored significantly lower in HBV knowledge than those who reported sound preventive practices. Of note, 38% of respondents reported positive HBsAg results to patients' employers and 25% reported positive results to patients' schools, thereby subjecting those with positive results to potential discriminatory practices.These results indicate that there is a need for development of effective educational programs to improve HBV knowledge among health professionals and the general public to avoid missed vaccination opportunities, reduce misconceptions, and eliminate discrimination based on chronic hepatitis B in China.

    View details for DOI 10.1186/1471-2458-10-98

    View details for Web of Science ID 000276447300002

    View details for PubMedID 20184740

  • Hidden Breast Cancer Disparities in Asian Women: Disaggregating Incidence Rates by Ethnicity and Migrant Status AMERICAN JOURNAL OF PUBLIC HEALTH Gomez, S. L., Quach, T., Horn-Ross, P. L., Pham, J. T., Cockburn, M., Chang, E. T., Keegan, T. H., Glaser, S. L., Clarke, C. A. 2010; 100: S125-S131

    Abstract

    We estimated trends in breast cancer incidence rates for specific Asian populations in California to determine if disparities exist by immigrant status and age.To calculate rates by ethnicity and immigrant status, we obtained data for 1998 through 2004 cancer diagnoses from the California Cancer Registry and imputed immigrant status from Social Security Numbers for the 26% of cases with missing birthplace information. Population estimates were obtained from the 1990 and 2000 US Censuses.Breast cancer rates were higher among US- than among foreign-born Chinese (incidence rate ratio [IRR] = 1.84; 95% confidence interval [CI] = 1.72, 1.96) and Filipina women (IRR = 1.32; 95% CI = 1.20, 1.44), but similar between US- and foreign-born Japanese women. US-born Chinese and Filipina women who were younger than 55 years had higher rates than did White women of the same age. Rates increased over time in most groups, as high as 4% per year among foreign-born Korean and US-born Filipina women. From 2000-2004, the rate among US-born Filipina women exceeded that of White women.These findings challenge the notion that breast cancer rates are uniformly low across Asians and therefore suggest a need for increased awareness, targeted cancer control, and research to better understand underlying factors.

    View details for DOI 10.2105/AJPH.2009.163931

    View details for Web of Science ID 000275937600025

    View details for PubMedID 20147696

  • Reproductive Factors and Non-Hodgkin Lymphoma Risk in the California Teachers Study PLOS ONE Prescott, J., Lu, Y., Chang, E. T., Sullivan-Halley, J., Henderson, K. D., Clarke, C. A., Ma, H., Templeman, C., Deapen, D., Bernstein, L. 2009; 4 (12)

    Abstract

    Non-Hodgkin lymphoma (NHL) is a malignancy etiologically linked to immunomodulatory exposures and disorders. Endogenous female sex hormones may modify immune function and influence NHL risk. Few studies have examined associations between reproductive factors, which can serve as surrogates for such hormonal exposures, and NHL risk by subtype.Women in the California Teachers Study cohort provided detailed data in 1995-1996 on reproductive history. Follow-up through 2007 identified 574 women with incident B-cell NHL. Hazard rate ratios (RR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models to assess associations between reproductive factors and all B-cell NHL combined, diffuse large B-cell lymphomas, follicular lymphomas, and B-cell chronic lymphocytic leukemias/small lymphocytic lymphomas. Pregnancy was marginally associated with lower risk of B-cell NHL (RR = 0.84, 95% CI = 0.68-1.04). Much of the reduction in risk was observed after one full-term pregnancy relative to nulligravid women (RR = 0.75, 95% CI = 0.54-1.06; P for trend <0.01), particularly for diffuse large B-cell lymphomas (P for trend = 0.13), but not among women who had only incomplete pregnancies. Age at first full-term pregnancy was marginally inversely associated with B-cell NHL risk overall (P for trend = 0.08) and for diffuse large B-cell lymphomas (P for trend = 0.056). Breast feeding was not associated with B-cell NHL risk overall or by subtype.Full-term pregnancy and early age at first full-term pregnancy account for most of the observed reduction in B-cell NHL risk associated with gravidity. Pregnancy-related hormonal exposures, including prolonged and high-level exposure to progesterone during a full-term pregnancy may inhibit development of B-cell NHL.

    View details for DOI 10.1371/journal.pone.0008135

    View details for Web of Science ID 000272828800026

    View details for PubMedID 19956586

  • Disparities in survival after Hodgkin lymphoma: a population-based study CANCER CAUSES & CONTROL Keegan, T. H., Clarke, C. A., Chang, E. T., Shema, S. J., Glaser, S. L. 2009; 20 (10): 1881-1892

    Abstract

    Survival after Hodgkin lymphoma (HL) is generally favorable, but may vary by patient demographic characteristics. The authors examined HL survival according to race/ethnicity and neighborhood socioeconomic status (SES), determined from residential census-block group at diagnosis. For 12,492 classical HL patients ? 15 years diagnosed in California during 1988-2006 and followed through 2007, we determined risk of overall and HL-specific death using Cox proportional hazards regression; analyses were stratified by age and Ann Arbor stage. Irrespective of disease stage, patients with lower neighborhood SES had worse overall and HL-specific survival than patients with higher SES. Patients with the lowest quintile of neighborhood SES had a 64% (patients aged 15-44 years) and 36% (? 45 years) increased risk of HL-death compared to patients with the highest quintile of SES; SES results were similar for overall survival. Even after adjustment for neighborhood SES, blacks and Hispanics had increased risks of HL-death 74% and 43% (15-44 years) and 40% and 17% (? 45 years), respectively, higher than white patients. The racial/ethnic differences in survival were evident for all stages of disease. These data provide evidence for substantial, and probably remediable, racial/ethnic and neighborhood SES disparities in HL outcomes.

    View details for DOI 10.1007/s10552-009-9382-3

    View details for Web of Science ID 000271809000010

    View details for PubMedID 19557531

  • Body Size, Recreational Physical Activity, and B-Cell Non-Hodgkin Lymphoma Risk Among Women in the California Teachers Study AMERICAN JOURNAL OF EPIDEMIOLOGY Lu, Y., Prescott, J., Sullivan-Halley, J., Henderson, K. D., Ma, H., Chang, E. T., Clarke, C. A., Horn-Ross, P. L., Ursin, G., Bernstein, L. 2009; 170 (10): 1231-1240

    Abstract

    Nutritional status and physical activity are known to alter immune function, which may be relevant to lymphomagenesis. The authors examined body size measurements and recreational physical activity in relation to risk of B-cell non-Hodgkin lymphoma (NHL) in the prospective California Teachers Study. Between 1995 and 2007, 574 women were diagnosed with incident B-cell NHL among 121,216 eligible women aged 22-84 years at cohort entry. Multivariable-adjusted relative risks and 95% confidence intervals were estimated by fitting Cox proportional hazards models for all B-cell NHL combined and for the 3 most common subtypes: diffuse large B-cell lymphoma, follicular lymphoma, and B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma. Height was positively associated with risk of all B-cell NHLs (for >1.70 vs. 1.61-1.65 m, relative risk = 1.50, 95% confidence interval: 1.16, 1.96) and chronic lymphocytic leukemia/small lymphocytic lymphoma (relative risk = 1.93, 95% confidence interval: 1.09, 3.41). Weight and body mass index at age 18 years were positive predictors of B-cell NHL risk overall. These findings indicate that greater height, which may reflect genetics, early life immune function, infectious exposures, nutrition, or growth hormone levels, may play a role in NHL etiology. Adiposity at age 18 years may be more relevant to NHL etiology than that in later life.

    View details for DOI 10.1093/aje/kwp268

    View details for Web of Science ID 000271379800005

    View details for PubMedID 19822569

  • Long-Term and Recent Recreational Physical Activity and Survival After Breast Cancer: The California Teachers Study CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION West-Wright, C. N., Henderson, K. D., Sullivan-Halley, J., Ursin, G., Deapen, D., Neuhausen, S., Reynolds, P., Chang, E., Ma, H., Bernstein, L. 2009; 18 (11): 2851-2859

    Abstract

    Long-term physical activity is associated with lower breast cancer risk. Little information exists on its association with subsequent survival.California Teachers Study cohort members provided information in 1995-1996 on long-term (high school through age 54 years) and recent (past 3 years) participation in moderate and strenuous recreational physical activities. The 3,539 women diagnosed with invasive breast cancer after cohort entry and through December 31, 2004, were followed through December 31, 2005. Of these, 460 women died, 221 from breast cancer. Moderate and strenuous physical activities were combined into low (3.0 h/wk/y), or high activity (>3.0 h/wk/y of either activity type). Multivariable relative risks (RR) and 95% confidence intervals (95% CI) for mortality were estimated using Cox proportional hazards methods, adjusting for race/ethnicity, estrogen receptor status, disease stage, and baseline information on comorbidities, body mass index, and caloric intake.Women with high or intermediate levels of long-term physical activity had lower risk of breast cancer death (RR, 0.53; 95% CI, 0.35-0.80; and RR, 0.65; 95% CI, 0.45-0.93, respectively) than women with low activity levels. These associations were consistent across estrogen receptor status and disease stage, but were confined to overweight women. Deaths due to causes other than breast cancer were related only to recent activity.Consistent long-term participation in physical activity before breast cancer diagnosis may lower risk of breast cancer death, providing further justification for public health strategies to increase physical activity throughout the lifespan.

    View details for DOI 10.1158/1055-9965.EPI-09-0538

    View details for Web of Science ID 000271562600008

    View details for PubMedID 19843680

  • Family history of breast cancer and all-cause mortality after breast cancer diagnosis in the Breast Cancer Family Registry BREAST CANCER RESEARCH AND TREATMENT Chang, E. T., Milne, R. L., Phillips, K., Figueiredo, J. C., Sangaramoorthy, M., Keegan, T. H., Andrulis, I. L., Hopper, J. L., Goodwin, P. J., O'Malley, F. P., Weerasooriya, N., Apicella, C., Southey, M. C., Friedlander, M. L., Giles, G. G., Whittemore, A. S., West, D. W., John, E. M. 2009; 117 (1): 167-176

    Abstract

    Although having a family history of breast cancer is a well established breast cancer risk factor, it is not known whether it influences mortality after breast cancer diagnosis. We studied 4,153 women with first primary incident invasive breast cancer diagnosed between 1991 and 2000, and enrolled in the Breast Cancer Family Registry through population-based sampling in Northern California, USA; Ontario, Canada; and Melbourne and Sydney, Australia. Cases were oversampled for younger age at diagnosis and/or family history of breast cancer. Carriers of germline mutations in BRCA1 or BRCA2 were excluded. Cases and their relatives completed structured questionnaires assessing breast cancer risk factors and family history of cancer. Cases were followed for a median of 6.5 years, during which 725 deaths occurred. Cox proportional hazards regression was used to evaluate associations between family history of breast cancer at the time of diagnosis and risk of all-cause mortality after breast cancer diagnosis, adjusting for established prognostic factors. The hazard ratios for all-cause mortality were 0.98 (95% confidence interval [CI] = 0.84-1.15) for having at least one first- or second-degree relative with breast cancer, and 0.85 (95% CI = 0.70-1.02) for having at least one first-degree relative with breast cancer, compared with having no such family history. Estimates did not vary appreciably when stratified by case or tumor characteristics. In conclusion, family history of breast cancer is not associated with all-cause mortality after breast cancer diagnosis for women without a known germline mutation in BRCA1 or BRCA2. Therefore, clinical management should not depend on family history of breast cancer.

    View details for DOI 10.1007/s10549-008-0255-3

    View details for Web of Science ID 000269005400020

    View details for PubMedID 19034644

  • Uncovering Disparities in Survival after Non-Small-Cell Lung Cancer among Asian/Pacific Islander Ethnic Populations in California CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Shema, S. J., Wakelee, H. A., Clarke, C. A., Gomez, S. L. 2009; 18 (8): 2248-2255

    Abstract

    Asians may have better survival after non-small-cell lung cancer (NSCLC) than non-Asians. However, it is unknown whether survival varies among the heterogeneous U.S. Asian/Pacific Islander (API) populations. Therefore, this study aimed to quantify survival differences among APIs with NSCLC. Differences in overall and disease-specific survival were analyzed in the California Cancer Registry among 16,577 API patients diagnosed with incident NSCLC between 1988 and 2007. Adjusted hazard ratios (HR) with 95% confidence intervals (95% CI) were estimated using Cox proportional hazards regression models with separate baseline hazards by disease stage. Despite better overall and disease-specific survival among APIs compared with non-Hispanic Whites, differences were evident across API populations. Among women, Japanese (overall survival HR, 1.16; 95% CI, 1.06-1.27) and APIs other than those in the six largest ethnic groups (other APIs; HR, 1.19; 95% CI, 1.07-1.33) had significantly poorer overall and disease-specific survival than Chinese. By contrast, South Asian women had significantly better survival than Chinese (HR, 0.79; 95% CI, 0.63-0.97). Among men, Japanese (HR, 1.15; 95% CI, 1.07-1.24), Vietnamese (HR, 1.07; 95% CI, 1.00-1.16), and other APIs (HR, 1.18; 95% CI, 1.08-1.28) had significantly poorer overall and disease-specific survival than Chinese. Other factors independently associated with poorer survival were lower neighborhood socioeconomic status, involvement with a non-university hospital, unmarried status, older age, and earlier year of diagnosis. APIs have significant ethnic differences in NSCLC survival that may be related to disparate lifestyles, biology, and especially health care access or use. To reduce the nationwide burden of lung cancer mortality, it is critical to identify and ameliorate hidden survival disparities such as those among APIs.

    View details for DOI 10.1158/1055-9965.EPI-09-0332

    View details for Web of Science ID 000268958600016

    View details for PubMedID 19622719

  • The Jade Ribbon Campaign: A Model Program for Community Outreach and Education to Prevent Liver Cancer in Asian Americans JOURNAL OF IMMIGRANT AND MINORITY HEALTH Chao, S. D., Chang, E. T., Le, P. V., Prapong, W., Kiernan, M., So, S. K. 2009; 11 (4): 281-290

    Abstract

    The Jade Ribbon Campaign (JRC) is a culturally targeted, community-based outreach program to promote the prevention, early detection, and management of chronic hepatitis B virus (HBV) infection and liver cancer among Asian Americans. In 2001, 476 Chinese American adults from the San Francisco Bay Area attended an HBV screening clinic and educational seminar. The prevalence of chronic HBV infection was 13%; only 8% of participants showed serologic evidence of protective antibody from prior vaccination. Participants reported low preventive action before the clinic, but after one year, 67% of those with chronic HBV infection had consulted a physician for liver cancer screening, and 78% of all participants had encouraged family members to be tested for HBV. The increase in HBV awareness, screening, and physician follow-up suggests that culturally aligned interventions similar to the JRC may help reduce the disproportionate burden of disease to chronic HBV infection among Asian Americans.

    View details for DOI 10.1007/s10903-007-9094-2

    View details for Web of Science ID 000281505100005

    View details for PubMedID 17990118

  • Recent trends in breast cancer incience in US white women by county-level urban/rural and poverty status BMC MEDICINE Hausauer, A. K., Keegan, T. H., Chang, E. T., Glaser, S. L., Howe, H., Clarke, C. A. 2009; 7

    Abstract

    Unprecedented declines in invasive breast cancer rates occurred in the United States between 2001 and 2004, particularly for estrogen receptor-positive tumors among non-Hispanic white women over 50 years. To understand the broader public health import of these reductions among previously unstudied populations, we utilized the largest available US cancer registry resource to describe age-adjusted invasive and in situ breast cancer incidence trends for non-Hispanic white women aged 50 to 74 years overall and by county-level rural/urban and poverty status.We obtained invasive and in situ breast cancer incidence data for the years 1997 to 2004 from 29 population-based cancer registries participating in the North American Association of Central Cancer Registries resource. Annual age-adjusted rates were examined overall and by rural/urban and poverty of patients' counties of residence at diagnosis. Joinpoint regression was used to assess trends by annual quarter of diagnosis.Between 2001 and 2004, overall invasive breast cancer incidence fell 13.2%, with greater reductions among women living in urban (-13.8%) versus rural (-7.5%) and low- (-13.0%) or middle- (-13.8%) versus high- (-9.6%) poverty counties. Most incidence rates peaked around 1999 then declined after second quarter 2002, although in rural counties, rates decreased monotonically after 1999. Similar but more attenuated patterns were seen for in situ cancers.Breast cancer rates fell more substantially in urban and low-poverty, affluent counties than in rural or high-poverty counties. These patterns likely reflect a major influence of reductions in hormone therapy use after July 2002 but cannot exclude possible effects due to screening patterns, particularly among rural populations where hormone therapy use was probably less prevalent.

    View details for DOI 10.1186/1741-7015-7-31

    View details for Web of Science ID 000268635200001

    View details for PubMedID 19558637

  • Prediagnosis Reproductive Factors and All-Cause Mortality for Women with Breast Cancer in the Breast Cancer Family Registry CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Phillips, K., Milne, R. L., West, D. W., Goodwin, P. J., Giles, G. G., Chang, E. T., Figueiredo, J. C., Friedlander, M. L., Keegan, T. H., Glendon, G., Apicella, C., O'Malley, F. P., Southey, M. C., Andrulis, I. L., John, E. M., Hopper, J. L. 2009; 18 (6): 1792-1797

    Abstract

    Studies have examined the prognostic relevance of reproductive factors before breast cancer diagnosis, but most have been small and their overall findings inconclusive. Associations between reproductive risk factors and all-cause mortality after breast cancer diagnosis were assessed with the use of a population-based cohort of 3,107 women of White European ancestry with invasive breast cancer (1,130 from Melbourne and Sydney, Australia; 1,441 from Ontario, Canada; and 536 from Northern California, United States). During follow-up with a median of 8.5 years, 567 deaths occurred. At recruitment, questionnaire data were collected on oral contraceptive use, number of full-term pregnancies, age at first full-term pregnancy, time from last full-term pregnancy to breast cancer diagnosis, breastfeeding, age at menarche, and menopause and menopausal status at breast cancer diagnosis. Hazard ratios for all-cause mortality were estimated with the use of Cox proportional hazards models with and without adjustment for age at diagnosis, study center, education, and body mass index. Compared with nulliparous women, those who had a child up to 2 years, or between 2 and 5 years, before their breast cancer diagnosis were more likely to die. The unadjusted hazard ratio estimates were 2.75 [95% confidence interval (95% CI), 1.98-3.83; P < 0.001] and 2.20 (95% CI, 1.65-2.94; P < 0.001), respectively, and the adjusted estimates were 2.25 (95% CI, 1.59-3.18; P < 0.001) and 1.82 (95% CI, 1.35-2.46; P < 0.001), respectively. When evaluating the prognosis of women recently diagnosed with breast cancer, the time since last full-term pregnancy should be routinely considered along with other established host and tumor prognostic factors, but consideration of other reproductive factors may not be warranted.

    View details for DOI 10.1158/1055-9965.EPI-08-1014

    View details for Web of Science ID 000266754100020

    View details for PubMedID 19505912

  • Polymorphic Variation in NFKB1 and Other Aspirin-Related Genes and Risk of Hodgkin Lymphoma CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Birmann, B. M., Kasperzyk, J. L., Conti, D. V., Kraft, P., Ambinder, R. F., Zheng, T., Mueller, N. E. 2009; 18 (3): 976-986

    Abstract

    We found that regular use of aspirin may reduce the risk of Hodgkin lymphoma (HL), a common cancer of adolescents and young adults in the United States. To explore possible biological mechanisms underlying this association, we investigated whether polymorphic variation in genes involved in nuclear factor-kappaB (NF-kappaB) activation and inhibition, other inflammatory pathways, and aspirin metabolism influences HL risk. Twenty single nucleotide polymorphisms (SNP) in seven genes were genotyped in DNA from 473 classical HL cases and 373 controls enrolled between 1997 and 2000 in a population-based case-control study in the Boston, Massachusetts, metropolitan area and the state of Connecticut. We selected target genes and SNPs primarily using a candidate-SNP approach and estimated haplotypes using the expectation-maximization algorithm. We used multivariable logistic regression to estimate odds ratios (OR) for associations with HL risk. HL risk was significantly associated with rs1585215 in NFKB1 (AG versus AA: OR, 2.1; 95% confidence interval, 1.5-2.9; GG versus AA: OR, 3.5; 95% confidence interval, 2.2-5.7, Ptrend=1.7x10(-8)) and with NFKB1 haplotypes (Pglobal=6.0x10(-21)). Similar associations were apparent across categories of age, sex, tumor EBV status, tumor histology, and regular aspirin use, although statistical power was limited for stratified analyses. Nominally significant associations with HL risk were detected for SNPs in NFKBIA and CYP2C9. HL risk was not associated with SNPs in IKKA/CHUK, PTGS2/COX2, UDP1A6, or LTC4S. In conclusion, genetic variation in the NF-kappaB pathway seems to influence risk of HL. Pooled studies are needed to detect any heterogeneity in the association with NF-kappaB across HL subgroups, including aspirin users and nonusers.

    View details for DOI 10.1158/1055-9965.EPI-08-1130

    View details for Web of Science ID 000264226100038

    View details for PubMedID 19223558

  • Family history of haematopoietic malignancies and non-Hodgkin's lymphoma risk in the California Teachers Study BRITISH JOURNAL OF CANCER Lu, Y., Sullivan-Halley, J., Cozen, W., Chang, E. T., Henderson, K., Ma, H., Deapen, D., Clarke, C., Reynolds, P., Neuhausen, S. L., Anton-Culver, H., Ursin, G., West, D., Bernstein, L. 2009; 100 (3): 524-526

    Abstract

    Family history of haematopoietic malignancies appears to be a risk factor for non-Hodgkin's lymphoma (NHL), but whether risk varies by family member's gender is unclear. Among 121 216 women participating in the prospective California Teachers Study, NHL risk varied by type of haematopoietic malignancy and gender of the relative.

    View details for DOI 10.1038/sj.bjc.6604881

    View details for Web of Science ID 000263074900013

    View details for PubMedID 19156148

  • 3 For Life: A Model Pilot Program to Prevent Hepatitis B Virus Infection and Liver Cancer in Asian and Pacific Islander Americans AMERICAN JOURNAL OF HEALTH PROMOTION Chang, E. T., Sue, E., Zola, J., So, S. K. 2009; 23 (3): 176-181

    Abstract

    3 For Life aims to increase hepatitis B virus (HBV) awareness and reduce the high prevalence of undiagnosed chronic HBV infection and susceptibility among Asian/Pacific Islander (API) adults.This pilot program offered low-cost HBV vaccination with free HBV testing targeted primarily at foreign-born Chinese adults.Semimonthly screening and vaccination clinics were held in San Francisco, California, for 1 year.A total of 1206 adults accessed the program.Participants paid a discounted fee for a full vaccine series against HBV, hepatitis A virus (HAV), or both. Participants also provided blood samples for HBV serologic testing. Test results, recommendations, and appointment reminders were provided by mail.We compared the probability of completing a recommended vaccine series by HBV serologic status and sociodemographic characteristics.Proportions were compared using multivariate logistic regression models.Nine percent of adults were chronically infected with HBV, and 53% were unprotected. In the latter group, 85% completed the HBV vaccine series. The probability of completing a recommended hepatitis vaccine series was similar across most sociodemographic groups, with slightly higher completion rates among middle-aged and Chinese participants.Lessons learned from this pilot program have been used toward successful replication in other cities, demonstrating that 3 For Life is an accessible, affordable, reproducible, and sustainable model to increase HBV awareness, testing, and prevention among API adults.

    View details for Web of Science ID 000262498400004

    View details for PubMedID 19149422

  • Eliminating the Threat of Chronic Hepatitis B in the Asian and Pacific Islander Community: A Call to Action ASIAN PACIFIC JOURNAL OF CANCER PREVENTION Chao, S. D., Chang, E. T., So, S. K. 2009; 10 (3): 507-512

    Abstract

    Chronic hepatitis B in the Asian and Pacific Islander (API) population is among our nation's greatest ethnic and racial health disparities. Despite comprising 4.3% of the population, API make up a disproportionate half of the 1.2-2 million Americans living with chronic hepatitis B. As many as two-thirds of API are not aware of their infection because they have not been tested. This lack of knowledge prevents them from undergoing life-saving liver cancer screening and potential treatment. Likewise, those not protected are unaware that they should be vaccinated. Instead, there is a pervasive lack of awareness among API and healthcare providers. New concerted public health actions are needed to eliminate this major health disparity.

    View details for Web of Science ID 000270750100033

    View details for PubMedID 19640200

  • Stopping a Silent Killer in the Underserved Asian and Pacific Islander Community: A Chronic Hepatitis B and Liver Cancer Prevention Clinic by Medical Students ASIAN PACIFIC JOURNAL OF CANCER PREVENTION Lin, S. Y., Chang, E. T., So, S. K. 2009; 10 (3): 383-386

    Abstract

    To assess and alleviate the burden of chronic hepatitis B virus (HBV) infection among low-income, uninsured Asian and Pacific Islanders (APIs) in San Jose, California.From 2007 to 2008, we provided free HBV testing and follow-up to 510 patients, 74% of whom were foreign-born Vietnamese. Patients were tested for hepatitis B surface antigen and surface antibody. Chronically infected patients who elected to undergo follow-up monitoring were evaluated for liver damage (ALT), liver cancer (AFP), and HBV replication (HBV DNA).Overall, 17% were chronically infected; 33% of these were unaware that they were infected. Of those who underwent follow-up monitoring, 100% had elevated ALT, 9% had elevated AFP, and 24% had HBV DNA levels that exceeded the threshold for treatment. Patients who were candidates for antiviral therapy were enrolled in drug assistance programs, and those with elevated AFP levels were referred for CT scans. Uninfected patients lacking protective antibodies were provided free HBV vaccinations.More liver cancer prevention in the medically underserved API community is needed, including universal screening for HBV and follow-up for those chronically infected.

    View details for Web of Science ID 000270750100011

    View details for PubMedID 19640178

  • Epidemiology of Non-small Cell Lung Cancer in Asian Americans Incidence Patterns Among Six Subgroups by Nativity JOURNAL OF THORACIC ONCOLOGY Raz, D. J., Gomez, S. L., Chang, E. T., Kim, J. Y., Keegan, T. H., Pham, J., Kukreja, J., Hiatt, R. A., Jablons, D. M. 2008; 3 (12): 1391-1397

    Abstract

    Differences in the epidemiology of lung cancer between Asians and non-Hispanic whites have brought to light the relative influences of genetic and environmental factors on lung cancer risk. We set out to describe the epidemiology of non-small cell lung cancer (NSCLC) among Asians living in California, and to explore the effects of acculturation on lung cancer risk by comparing lung cancer rates between U.S.-born and foreign-born Asians.Age-adjusted incidence rates of NSCLC were calculated for Chinese, Filipino, Japanese, Korean, Vietnamese, and South Asians in California between 1988 and 2003 using data from the California Cancer Registry. Incidence rates were calculated and stratified by sex and nativity. We analyzed population-based tobacco smoking prevalence data to determine whether differences in rates were associated with prevalence of tobacco smoking.Asians have overall lower incidence rates of NSCLC compared with whites (29.8 and 57.7 per 100,000, respectively). South Asians have markedly low rates of NSCLC (12.0 per 100,000). Foreign-born Asian men and women have an approximately 35% higher rate of NSCLC than U.S.-born Asian men and women. The incidence pattern by nativity is consistent with the population prevalence of smoking among Asian men; however, among women, the prevalence of smoking is higher among U.S.-born, which is counter to their incidence patterns.Foreign-born Asians have a higher rate of NSCLC than U.S.-born Asians, which may be due to environmental tobacco smoke or nontobacco exposures among women. South Asians have a remarkably low rate of NSCLC that approaches white levels among the U.S.-born. More studies with individual-level survey data are needed to identify the specific environmental factors associated with differential lung cancer risk occurring with acculturation among Asians.

    View details for Web of Science ID 000261712300006

    View details for PubMedID 19057262

  • Lifetime total physical activity and prostate cancer risk: a population-based case-control study in Sweden EUROPEAN JOURNAL OF EPIDEMIOLOGY Wiklund, F., Lageros, Y. T., Chang, E., Balter, K., Johansson, J., Adami, H., Gronberg, H. 2008; 23 (11): 739-746

    Abstract

    The etiologic role of physical activity in prostate cancer development is unclear. We assessed the association between lifetime total physical activity and prostate cancer risk in a Swedish population-based case-control study comprising 1,449 incident prostate cancer cases and 1,118 unaffected population controls. Information regarding physical activity was obtained via a self-administered questionnaire assessing occupational, household, and recreational activity separately at various ages throughout an individual's lifetime. Clinical data (TNM-classification, Gleason sum and PSA) was obtained from linkage to the National Prostate Cancer Registry. Overall, we observed no association between lifetime total physical activity and prostate cancer risk (odds ratio [OR] = 1.04, 95% confidence interval [CI] = 0.77-1.41 for > or =49.7 vs. <41.9 metabolic equivalent-hours per day). There was a significantly increased risk of prostate cancer in the most active men compared with the least active men in household (OR = 1.44, 95% CI = 1.08-1.92) and recreational physical activity (OR = 1.56, 95% CI = 1.16-2.10). Comparing the most active with the least active men, total physical activity was not associated with either localized disease (OR = 0.95, 95% CI = 0.67-1.34) or advanced disease (OR = 1.19, 95% CI = 0.83-1.71). These findings do not support the hypothesis that physical activity uniformly protects against prostate cancer development.

    View details for DOI 10.1007/s10654-008-9294-7

    View details for Web of Science ID 000261691000005

    View details for PubMedID 18931922

  • Serum YKL-40 and Interleukin 6 Levels in Hodgkin Lymphoma CLINICAL CANCER RESEARCH Biggar, R. J., Johansen, J. S., Smedby, K. E., Rostgaard, K., Chang, E. T., Adami, H., Glimelius, B., Molin, D., Hamilton-Dutoit, S., Melbye, M., Hjalgrim, H. 2008; 14 (21): 6974-6978

    Abstract

    Serum levels of the inflammatory markers YKL-40 and interleukin 6 (IL-6) are increased in many conditions, including cancers. We examined serum YKL-40 and IL-6 levels in patients with Hodgkin lymphoma, a tumor with strong immunologic reaction to relatively few tumor cells, especially in nodular sclerosis Hodgkin lymphoma.We analyzed Danish and Swedish patients with incident Hodgkin lymphoma (N=470) and population controls from Denmark (n=245 for YKL-40; n=348 for IL-6). Serum YKL-40 and IL-6 levels were determined by ELISA, and log-transformed data were analyzed by linear regression, adjusting for age and sex.Serum levels of YKL-40 and IL-6 increased in Hodgkin lymphoma patients compared with controls (YKL-40, 3.6-fold; IL-6, 8.3-fold; both, P<0.0001). In pretreatment samples from pretreatment Hodgkin lymphoma patients (n=176), levels were correlated with more advanced stages (P(trend), 0.0001 for YKL-40 and 0.013 for IL-6) and in those with B symptoms; however, levels were similar in nodular sclerosis and mixed cellularity subtypes, by EBV status, and in younger (<45 years old) and older patients. Patients tested soon after treatment onset had significantly lower levels than pretreatment patients; however, even >or=6 months after treatment onset, serum YKL-40 and IL-6 levels remained significantly increased compared with controls. In patients who died (n=12), pretreatment levels for YKL-40 and IL-6 were higher than in survivors, although not statistically significantly.Serum YKL-40 and IL-6 levels were increased in untreated Hodgkin lymphoma patients and those with more advanced stages but did not differ significantly by Hodgkin lymphoma histology. Following treatment, serum levels were significantly lower.

    View details for DOI 10.1158/1078-0432.CCR-08-1026

    View details for Web of Science ID 000260732200031

    View details for PubMedID 18980992

  • Racial/ethnic variation in EBV-positive classical Hodgkin lymphoma in California populations INTERNATIONAL JOURNAL OF CANCER Glaser, S. L., Gulley, M. L., Clarke, C. A., Keegan, T. H., Chang, E. T., Shema, S. J., Craig, F. E., DiGiuseppe, J. A., Dorfman, R. F., Mann, R. B., Anton-Culver, H., Ambinder, R. F. 2008; 123 (7): 1499-1507

    Abstract

    Epstein-Barr virus (EBV) is detected in the tumor cells of some but not all Hodgkin lymphoma (HL) patients, and evidence indicates that EBV-positive and -negative HL are distinct entities. Racial/ethnic variation in EBV-positive HL in international comparisons suggests etiologic roles for environmental and genetic factors, but these studies used clinical series and evaluated EBV presence by differing protocols. Therefore, we evaluated EBV presence in the tumors of a large (n = 1,032), racially and sociodemographically diverse series of California incident classical HL cases with uniform pathology re-review and EBV detection methods. Tumor EBV-positivity was associated with Hispanic and Asian/Pacific Islander (API) but not black race/ethnicity, irrespective of demographic and clinical factors. Complex race-specific associations were observed between EBV-positive HL and age, sex, histology, stage, neighborhood socioeconomic status (SES), and birth place. In Hispanics, EBV-positive HL was associated not only with young and older age, male sex, and mixed cellularity histology, but also with foreign birth and lower SES in females, suggesting immune function responses to correlates of early childhood experience and later environmental exposures, respectively, as well as of pregnancy. For APIs, a lack of association with birth place may reflect the higher SES of API than Hispanic immigrants. In blacks, EBV-positive HL was associated with later-stage disease, consistent with racial/ethnic variation in certain cytokine polymorphisms. The racial/ethnic variation in our findings suggests that EBV-positive HL results from an intricate interplay of early- and later-life environmental, hormonal, and genetic factors leading to depressed immune function and poorly controlled EBV infection.

    View details for DOI 10.1002/ijc.23741

    View details for Web of Science ID 000258892500003

    View details for PubMedID 18646185

  • Sex differences in lung-cancer susceptibility: a smoke screen? LANCET ONCOLOGY Wakelee, H. A., Gomez, S. L., Chang, E. T. 2008; 9 (7): 609-610

    View details for Web of Science ID 000257527400006

    View details for PubMedID 18598927

  • Borrelia infection and risk of non-Hodgkin lymphoma BLOOD Schollkopf, C., Melbye, M., Munksgaard, L., Smedby, K. E., Rostgaard, K., Glimelius, B., Chang, E. T., Roos, G., Hansen, M., Adami, H., Hjalgrim, H. 2008; 111 (12): 5524-5529

    Abstract

    Reports of the presence of Borrelia burgdorferi DNA in malignant lymphomas have raised the hypothesis that infection with B. burgdorferi may be causally related to non-Hodgkin lymphoma (NHL) development. We conducted a Danish-Swedish case-control study including 3055 NHL patients and 3187 population controls. History of tick bite or Borrelia infection was ascertained through structured telephone interviews and through enzyme-linked immunosorbent assay serum analyses for antibodies against B. burgdorferi in a subset of 1579 patients and 1358 controls. Statistical associations with risk of NHL, including histologic subtypes, were assessed by logistic regression. Overall risk of NHL was not associated with self-reported history of tick bite (odds ratio [OR] = 1.0; 95% confidence interval: 0.9-1.1), Borrelia infection (OR = 1.3 [0.96-1.8]) or the presence of anti-Borrelia antibodies (OR = 1.3 [0.9-2.0]). However, in analyses of NHL subtypes, self-reported history of B. burgdorferi infection (OR = 2.5 [1.2-5.1]) and seropositivity for anti-Borrelia antibodies (OR = 3.6 [1.8-7.4]) were both associated with risk of mantle cell lymphoma. Notably, this specific association was also observed in persons who did not recall Borrelia infection yet tested positive for anti-Borrelia antibodies (OR = 4.2 [2.0-8.9]). Our observations suggest a previously unreported association between B. burgdorferi infection and risk of mantle cell lymphoma.

    View details for DOI 10.1182/blood-2007-08-109611

    View details for Web of Science ID 000256786500023

    View details for PubMedID 18424667

  • Incomplete pregnancy is not associated with breast cancer risk: the California Teachers Study CONTRACEPTION Henderson, K. D., Sullivan-Halley, J., Reynolds, P., Horn-Ross, P. L., Clarke, C. A., Chang, E. T., Neuhausen, S., Ursin, G., Bernstein, L. 2008; 77 (6): 391-396

    Abstract

    Early studies of incomplete pregnancy and development of breast cancer suggested that induced abortion might increase risk. Several large prospective studies, which eliminate recall bias, did not detect associations, but this relationship continues to be debated.To further inform this important question, we examined invasive breast cancer as it relates to incomplete pregnancy, including total number of induced abortions, age at first induced abortion and total number of miscarriages among women participating in the ongoing California Teachers Study (CTS) cohort. Incomplete pregnancy was self-reported on the CTS baseline questionnaire in 1995-1996. Incident breast cancers were ascertained in 3324 women through 2004 via linkage with the California Cancer Registry.Using Cox multivariable regression, we found no statistically significant association between any measure of incomplete pregnancy and breast cancer risk among nulliparous or parous women.These results provide strong evidence that there is no relationship between incomplete pregnancy and breast cancer risk.

    View details for DOI 10.1016/j.contraception.2008.02.004

    View details for Web of Science ID 000256136200002

    View details for PubMedID 18477486

  • Dietary patterns and risk of ovarian cancer in the California Teachers Study Cohort NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL Chang, E. T., Lee, V. S., Canchola, A. J., Dalvi, T. B., Clarke, C. A., Reynolds, P., Purdie, D. M., Stram, D. O., West, D. W., Ziogas, A., Bernstein, L., Horn-Ross, P. L. 2008; 60 (3): 285-291

    Abstract

    Previous studies have examined the association between individual foods or nutrients, but not overall diet, and ovarian cancer risk. To account for the clustering of foods in the diet, we investigated the association between dietary patterns and risk of ovarian cancer in the prospective California Teachers Study cohort. Of 97,292 eligible women who completed the baseline dietary assessment in 1995-1996, 311 women developed epithelial ovarian cancer on or before December 31, 2004. Based on principal components analysis, 5 major dietary patterns were identified and termed plant-based, high-protein/high-fat, high-carbohydrate, ethnic, and salad-and-wine. Multivariable Cox proportional hazards regression analysis was used to estimate associations between these dietary patterns and risk of incident ovarian cancer. Most of the dietary patterns were not significantly associated with ovarian cancer risk. However, women who followed a plant-based diet had higher risk; comparing those in the top quintile of plant-based food intake with those in the lowest quintile, the relative risk of ovarian cancer was 1.65 (95% confidence interval = 1.07-2.54; P(trend) = 0.03). Associations with the 5 dietary patterns did not vary by known ovarian cancer risk factors or other behavioral or sociodemographic characteristics. Overall, our results show no convincing associations between dietary patterns and ovarian cancer risk.

    View details for DOI 10.1080/01635580701733091

    View details for Web of Science ID 000256439800001

    View details for PubMedID 18444162

  • Hepatitis C infection and risk of malignant lymphoma INTERNATIONAL JOURNAL OF CANCER Schoellkopf, C., Smedby, K. E., Hjalgrim, H., Rostgaard, K., Panum, I., Vinner, L., Chang, E. T., Glimelius, B., Porwit, A., Sundstroem, C., Hansen, M., Adami, H., Melbye, M. 2008; 122 (8): 1885-1890

    Abstract

    The association between hepatitis C virus (HCV) infection and risk of malignant lymphoma remains controversial, perhaps due to small-sized studies and low prevalence of HCV in the general population. On the basis of a large Danish-Swedish population-based case-control study, 2,819 lymphoma patients and 1,856 controls of second-generation Danish-Swedish origin were screened for HCV infection using an enzyme-linked immunosorbent assay and a confirming recombinant immunoblot assay (RIBA) test. Positive samples were tested with real-time PCR for the presence of HCV RNA. The association between HCV infection and risk of malignant lymphoma was assessed by logistic regression. When intermediate RIBA test results were interpreted as positive, anti-HCV antibody positivity was associated with a nonsignificant increased risk of non-Hodgkin lymphoma (NHL) overall (odds ratio (OR) = 2.2; 95% confidence interval (CI) 0.9-5.3; n = 20 cases), of B-cell lymphomas combined (OR = 2.4 [1.0-5.8]; n = 20) and of lymphoplasmacytic lymphoma (OR = 5.2 [1.0-26.4]; n = 2). No patients with T-cell or Hodgkin lymphoma were HCV-positive. A more conservative definition of HCV positivity (disregarding intermediate RIBA results) resulted in an OR = 1.6 (0.3-8.5; n = 5) for NHL overall. When the definition was further restricted to require HCV RNA positivity, OR was 1.7 (0.2-16.2; n = 3) for NHL overall. Our findings from a population with a low prevalence of HCV suggest a positive association between HCV and risk of NHL, in particular of B-cell origin.

    View details for DOI 10.1002/ijc.23416

    View details for Web of Science ID 000254068300030

    View details for PubMedID 18271005

  • Attitudes toward Hepatitis B and Liver Cancer Prevention among Chinese Americans in the San Francisco Bay Area, California ASIAN PACIFIC JOURNAL OF CANCER PREVENTION Chang, E. T., Nguyen, B. H., So, S. K. 2008; 9 (4): 605-613

    Abstract

    Chronic hepatitis B and associated liver cancer constitute important health threats with disparity among Asian/Pacific Islander Americans (APIs). However, many APIs are unaware of and unprotected against these diseases.To inform the development of community-based programs to increase hepatitis B and liver cancer awareness and prevention among APIs, we conducted a series of qualitative focus groups in 2007 to identify motivations and deterrents related to hepatitis B education, testing, and vaccination among San Francisco Bay Area Chinese Americans. Six focus groups were held in Cantonese, English, or Mandarin for women or men, respectively. Recorded transcripts were transcribed, translated, and then coded by consensus.Factors that motivated individuals to be tested for hepatitis B included peace of mind, prevention of transmission to others, informed decision-making ability, convenience, and pre-vaccination screening. Primary motivations for hepatitis B vaccination were protection of future health and avoidance of hepatitis B. However, factors that discouraged people from testing or vaccination included costs, lack of health insurance, fear of side effects, worries about reliability or efficacy, poor patient-doctor communication, reliance on professional opinion, apparent good health, inconvenience, and personal preference. Individuals were generally in favor of informing relatives and friends about hepatitis B testing and vaccination, and offered several reasons for and against educating others about these activities.In summary, our study identifies common attitudes and influences regarding the decision to take preventive action against hepatitis B and liver cancer. These findings can be applied toward the design of more effective educational and outreach materials and programs for Chinese Americans and possibly other APIs.

    View details for Web of Science ID 000269713600014

    View details for PubMedID 19256747

  • Building partnerships with Traditional Chinese Medicine Practitioners to increase hepatitis B awareness and prevention JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE Chang, E. T., Lin, S. Y., Sue, E., Bergin, M., Su, J., So, S. K. 2007; 13 (10): 1125-1127

    Abstract

    The annual Hepatitis B Prevention and Education Symposium aims to develop partnerships between non-Western and Western health care providers to prevent chronic hepatitis B virus (HBV) infection and death from liver cancer among Asians and Pacific Islanders (APIs).Each year from 2004 through 2007, we partnered with professional, academic, and community-based organizations to organize an educational symposium for Traditional Chinese Medicine practitioners and acupuncturists in California. Participants completed pre- and postsymposium surveys assessing knowledge about HBV and liver cancer.The symposia were held in San Francisco, Los Angeles, and Stanford, California.Over 1000 participants attended the four symposia combined; most were born in Asia.Symposium activities included educational lectures and games, presentation of a physician's guide to HBV management, and case studies.Chi-square tests were used to compare the proportion of correct responses to each knowledge-based question, as well as the total number of correct responses, before and after the symposium.Knowledge about HBV and liver cancer was low prior to the symposium. The proportion of correct responses to the most commonly mistaken questions increased significantly at the conclusion of each symposium. The total number of correct responses rose from below 60% to above 75% each year.Similar educational symposia targeting health care providers who serve API patients can improve HBV and liver cancer awareness and prevention throughout the API community.

    View details for DOI 10.1089/acm.2007.0655

    View details for Web of Science ID 000252247200014

    View details for PubMedID 18166125

  • Childhood social environment and risk of non-hodgkin lymphoma in adults CANCER RESEARCH Smedby, K. E., Hjalgrim, H., Chang, E. T., Rostgaard, K., Glimelius, B., Adami, H., Melbye, M. 2007; 67 (22): 11074-11082

    Abstract

    Better hygiene and sanitation and decreasing family size parallel the increasing incidence of non-Hodgkin lymphoma (NHL) in many populations around the world. However, whether sibship size, birth order, and crowding are related to adult NHL risk is not clear. We investigated how family structure and childhood social environment were related to the risk of NHL and NHL subtypes in a large Scandinavian population-based case control study with 6,242 participants aged 18 to 74 years. Detailed exposure information was obtained through telephone interviews. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using logistic regression, and all statistical tests were two-sided. Having four or more siblings was associated with a moderately increased risk of NHL, compared with having no siblings (OR 1.34, 95% CI 1.11-1.62, P(trend) < 0.001). Having four or more older siblings was associated with a similar risk increase (OR 1.33, 95% CI 1.12-1.59, P(trend) = 0.003) compared with being the oldest, whereas number of younger siblings was unrelated overall. The associations were independent of other environmental exposures and did not vary by country, age, or sex. High household crowding was also positively associated with risk of NHL. Results were slightly stronger for diffuse large B-cell and T-cell lymphomas than for other major NHL subtypes. Our findings add to the evidence that large sibship size, late birth order, and childhood crowding are associated with an elevated risk of NHL. Effect mechanisms may be related to early age at onset and high frequency of specific infections or total microbial exposure in childhood.

    View details for DOI 10.1158/0008-5472.CAN-07-1751

    View details for Web of Science ID 000251044000054

    View details for PubMedID 18006854

  • Re: "Ten largest racial and ethnic health disparities in the United States based on healthy people 2010 objectives" AMERICAN JOURNAL OF EPIDEMIOLOGY Chang, E. T., So, S. K. 2007; 166 (9): 1105-1106

    View details for DOI 10.1093/aje/kwm26

    View details for Web of Science ID 000250400700016

    View details for PubMedID 17881381

  • Sex- and kindred-specific familial risk of non-Hodgkin's lymphoma CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Czene, K., Adami, H., Chang, E. T. 2007; 16 (11): 2496-2499

    Abstract

    A family history of non-Hodgkin's lymphoma (NHL) confers increased risk of NHL, but it is unknown whether the excess risk in males and females varies by the sex or kinship of the affected relative. We linked nationwide Swedish registries to identify parents and siblings of NHL patients who developed NHL between January 1, 1961 and December 31, 2002. In males, parental risks were approximately the same from fathers and mothers, whereas sibling risks were higher from brothers [standardized incidence ratio (SIR), 1.8; 95% confidence interval (95% CI), 1.0-2.9] than sisters (SIR, 0.9; 95% CI, 0.2-1.9). In females, parental and sibling risks were higher from same-sex relatives (SIR from mothers, 1.9; 95% CI, 1.2-2.7; SIR from sisters, 6.3; 95% CI, 4.0-9.3) than from opposite-sex relatives (SIR from fathers, 1.2; 95% CI, 0.7-1.9; SIR from brothers, 0.7; 95% CI, 0.2-1.6). These findings did not vary substantially by the age of diagnosis of the offspring. Risk of NHL in offspring was also increased among those with a parent diagnosed with multiple myeloma or leukemia. The relative risk of NHL among those with a parent diagnosed with any hematopoietic cancer was 1.5 (95% CI, 1.4-1.7) and that for having a sibling with any hematopoietic cancer was also 1.5 (95% CI, 1.2-1.9). Our results suggest that part of the familial risk of NHL may be attributable to shared environmental exposures, particularly between same-sex siblings.

    View details for DOI 10.1158/1055-9965.EPI-07-0163

    View details for Web of Science ID 000251123500046

    View details for PubMedID 18006943

  • Why we should routinely screen Asian American adults for hepatitis B: A cross-sectional study of Asians in California HEPATOLOGY Lin, S. Y., Chang, E. T., So, S. K. 2007; 46 (4): 1034-1040

    Abstract

    Chronic hepatitis B virus (HBV) infection is a serious liver disease that, if left undiagnosed or without appropriate medical management, is associated with a 25% chance of death from cirrhosis or liver cancer. To study the demographics and prevalence of chronic HBV infection and HBV vaccination in the Asian American population, we provided free HBV serological screening and administered a survey to 3163 Asian American adult volunteers in the San Francisco Bay Area between 2001 and 2006. Of those screened, 8.9% were chronically infected with HBV. Notably, one-half to two-thirds (65.4%) of the chronically infected adults were unaware that they were infected. Of those who were not chronically infected, 44.8% lacked protective antibodies against HBV and were likely susceptible to future infection. Men were twice as likely as women to be chronically infected (12.1% versus 6.4%). Asian Americans born in East Asia, Southeast Asia, or the Pacific Islands were 19.4 times more likely to be chronically infected than those born in the United States. Self-reporting of prior vaccination was unreliable to assess protection against HBV. Among the 12% who reported having been vaccinated, 5.2% were chronically infected, and 20.3% lacked protective antibodies.Given the high prevalence of unrecognized chronic HBV infection in the Asian American population, we call for healthcare providers to routinely screen Asian adults for HBV, regardless of their vaccination status. Those who test positive should be provided with culturally appropriate information to prevent disease transmission and proper medical management to reduce their risk of liver disease.

    View details for DOI 10.1002/hep.21784

    View details for Web of Science ID 000249910500013

    View details for PubMedID 17654490

  • Cigarette smoking and risk of Hodgkin lymphoma: A population-based case-control study CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Hjalgrim, H., Ekstrom-Smedby, K., Rostgaard, K., Amini, R., Molin, D., Hamilton-Dutoit, S., Schollkopf, C., Chang, E. T., Ralfkiaer, E., Adami, H., Glimelius, B., Melbye, M. 2007; 16 (8): 1561-1566

    Abstract

    Studies have inconsistently reported an association between tobacco smoking and Hodgkin lymphoma (HL) risk. The conflicting finding may reflect etiologic heterogeneity between HL subtypes, warranting further characterization of the relationship.We collected information on tobacco-smoking habits in 586 classic HL cases and 3,187 population controls in a Danish-Swedish case-control study. HL EBV status was established for 499 cases by standard techniques. Odds ratios (OR) for an association with cigarette smoking were calculated by logistic regression for HL overall and stratified by age, sex, major histology subtypes, and tumor EBV status, adjusting for known confounders.Compared with never smokers, current cigarette smokers were at an increased overall HL risk [adjusted OR, 1.57; 95% confidence interval (95% CI), 1.22-2.03]. The association was strongest for EBV-positive HL (adjusted OR, 2.36; 95% CI, 1.51-3.71), but also applied to EBV-negative HL (adjusted OR, 1.43; 95% CI, 1.05-1.97; P(homogeneity EBV-pos) versus P(homogeneity EBV-neg) = 0.04). The association did not vary appreciably by age, sex, or histologic subtype, the apparent EBV-related difference present in all strata. There was no evidence of a dose-response pattern, whether by age at smoking initiation, daily cigarette consumption, number of years smoking, or cumulative number of cigarettes smoked. Similar results were obtained in analyses using non-HL patients (n = 3,055) participating in the founding study as comparison group.The observed association between cigarette smoking and HL risk is consistent with previous findings and biologically credible. Although not easily dismissed as an artifact, the limited evidence of a dose-response pattern renders the overall evidence of causality weak.

    View details for DOI 10.1158/1055-9965.EPI-07-0094

    View details for Web of Science ID 000248715100007

    View details for PubMedID 17684129

  • The burden of liver cancer in Asians and Pacific Islanders in the greater San Francisco Bay Area, 1990 through 2004 CANCER Chang, E. T., Keegan, T. H., Gomez, S. L., Le, G. M., Clarke, C. A., So, S. K., Glaser, S. L. 2007; 109 (10): 2100-2108

    Abstract

    To the authors' knowledge, no previous U.S. study has examined time trends in the incidence rate of liver cancer in the high-risk Asian/Pacific Islander population. In this study, liver cancer incidence trends were evaluated in Chinese, Filipino, Japanese, Korean, and Vietnamese men and women in the Greater San Francisco Bay Area of California between 1990 and 2004.Populations at risk were estimated by using the cohort-component demographic method. Annual percentage changes (APCs) in age-adjusted incidence rates of primary liver cancer among Asians/Pacific Islanders in the Greater Bay Area Cancer Registry were calculated by using joinpoint regression analysis.The incidence rate of liver cancer between 1990 and 2004 did not change significantly in Asian/Pacific Islander men or women overall. However, the incidence rate declined, although the decline was not statistically significant, among Chinese men (APC, -1.6%; 95% confidence interval [95% CI], -3.4-0.3%), Japanese men (APC, -4.9%; 95% CI, -10.7-1.2%), and Japanese women (APC, -3.6%; 95% CI, -8.9-2%). Incidence rates remained consistently high for Vietnamese, Korean, and Filipino men and women. Trends in the incidence rate of hepatocellular carcinoma were comparable to those for liver cancer. Although disparities in liver cancer incidence between Asians/Pacific Islanders and other racial/ethnic groups diminished between the period from 1990 through 1994 and the period from 2000 through 2004, the disparities among Asian subgroups increased.Liver cancer continues to affect Asian/Pacific Islander Americans disproportionately, with consistently high incidence rates in most subgroups. Culturally targeted prevention methods are needed to reduce the high rates of liver cancer in this growing population in the U.S.

    View details for DOI 10.1002/cncr.22642

    View details for Web of Science ID 000246252800024

    View details for PubMedID 17385214

  • Diet and risk of ovarian cancer in the California teachers study cohort AMERICAN JOURNAL OF EPIDEMIOLOGY Chang, E. T., Lee, V. S., Canchola, A. J., Clarke, C. A., Purdie, D. M., Reynolds, P., Anton-Culver, H., Bernstein, L., Deapen, D., Peel, D., Pinder, R., Ross, R. K., Stram, D. O., West, D. W., Wright, W., Ziogas, A., Horn-Ross, P. L. 2007; 165 (7): 802-813

    Abstract

    Dietary phytochemical compounds, including isoflavones and isothiocyanates, may inhibit cancer development but have not yet been examined in prospective epidemiologic studies of ovarian cancer. The authors have investigated the association between consumption of these and other nutrients and ovarian cancer risk in a prospective cohort study. Among 97,275 eligible women in the California Teachers Study cohort who completed the baseline dietary assessment in 1995-1996, 280 women developed invasive or borderline ovarian cancer by December 31, 2003. Multivariable Cox proportional hazards regression, with age as the timescale, was used to estimate relative risks and 95% confidence intervals; all statistical tests were two sided. Intake of isoflavones was associated with lower risk of ovarian cancer. Compared with the risk for women who consumed less than 1 mg of total isoflavones per day, the relative risk of ovarian cancer associated with consumption of more than 3 mg/day was 0.56 (95% confidence interval: 0.33, 0.96). Intake of isothiocyanates or foods high in isothiocyanates was not associated with ovarian cancer risk, nor was intake of macronutrients, antioxidant vitamins, or other micronutrients. Although dietary consumption of isoflavones may be associated with decreased ovarian cancer risk, most dietary factors are unlikely to play a major role in ovarian cancer development.

    View details for DOI 10.1093/aje/kwk065

    View details for Web of Science ID 000244959600010

    View details for PubMedID 17210953

  • Infectious mononucleosis, childhood social environment, and risk of Hodgkin lymphoma CANCER RESEARCH Hjalgrim, H., Smedby, K. E., Rostgaard, K., Molin, D., Hamilton-Dutoit, S., Chang, E. T., Ralfkiaer, E., Sundstrom, C., Adami, H., Glimelius, B., Melbye, M. 2007; 67 (5): 2382-2388

    Abstract

    Infectious mononucleosis (IM) has been associated with an increased risk of Hodgkin lymphoma (HL), implicating a role for Epstein-Barr virus (EBV) in HL development. Although essential to the understanding of the association, it has remained uncertain if the relationship is restricted to the EBV-positive subset of HL. We collected information on mononucleosis history and childhood socioenvironmental characteristics in a population-based study of 586 patients with classic HL and 3,187 controls in Denmark and Sweden. Tumor EBV status was established for 499 cases by immunohistochemistry and in situ hybridization techniques. Odds ratios (OR) for the relationship between HL risk and mononucleosis and other risk factors were estimated by logistic regression for HL in younger (18-44 years) and older (45-74 years) adults, overall and by tumor EBV status. All analyses were adjusted for country-specific measures of maternal education and mononucleosis history. IM was associated with an increased risk of EBV-positive [OR, 3.23; 95% confidence interval (95% CI) 1.89-5.55] but not EBV-negative HL (OR, 1.35; 95% CI, 0.86-2.14). Risk of EBV-positive HL varied with time since IM and was particularly pronounced in younger adults (OR, 3.96; 95% CI, 2.19-7.18). IM-associated lymphomas occurred with a median of 2.9 years (1.8-4.9 years) after infection. The EBV specificity of the IM association was corroborated by a case-case comparison of IM history between younger adult EBV-positive and EBV-negative HL patients (OR(IM EBV+ HL versus EBV- HL), 2.68; 95% CI, 1.40-5.12). We found further evidence that IM is associated only with EBV-positive HL. This finding is compatible with the notion that EBV-positive and EBV-negative HL may have different etiologies.

    View details for DOI 10.1158/0008-5472.CAN-06-3566

    View details for Web of Science ID 000244738100062

    View details for PubMedID 17332371

  • Lung cancer incidence in never smokers JOURNAL OF CLINICAL ONCOLOGY Wakelee, H. A., Chang, E. T., Gomez, S. L., Keegan, T. H., Feskanich, D., Clarke, C. A., Holmberg, L., Yong, L. C., Kolonel, L. N., Gould, M. K., West, D. W. 2007; 25 (5): 472-478

    Abstract

    Lung cancer is a leading cause of cancer death worldwide. Although smoking remains the predominant cause of lung cancer, lung cancer in never smokers is an increasingly prominent public health issue. However, data on this topic, particularly lung cancer incidence rates in never smokers, are limited.We reviewed the existing literature on lung cancer incidence and mortality rates among never smokers and present new data regarding rates in never smokers from the following large, prospective cohorts: Nurses' Health Study; Health Professionals Follow-Up Study; California Teachers Study; Multiethnic Cohort Study; Swedish Lung Cancer Register in the Uppsala/Orebro region; and First National Health and Nutrition Examination Survey Epidemiologic Follow-Up Study.Truncated age-adjusted incidence rates of lung cancer among never smokers age 40 to 79 years in these six cohorts ranged from 14.4 to 20.8 per 100,000 person-years in women and 4.8 to 13.7 per 100,000 person-years in men, supporting earlier observations that women are more likely than men to have non-smoking-associated lung cancer. The distinct biology of lung cancer in never smokers is apparent in differential responses to epidermal growth factor receptor inhibitors and an increased prevalence of adenocarcinoma histology in never smokers.Lung cancer in never smokers is an important public health issue, and further exploration of its incidence patterns, etiology, and biology is needed.

    View details for DOI 10.1200/JCO.2006.07.2983

    View details for Web of Science ID 000244176000003

    View details for PubMedID 17290054

  • Making sense of seasonal fluctuations in lymphoma diagnosis LEUKEMIA & LYMPHOMA Chang, E. T., Clarke, C. A., Glaser, S. L. 2007; 48 (2): 223-224

    View details for DOI 10.1080/10428190601158662

    View details for Web of Science ID 000244528300005

    View details for PubMedID 17325879

  • Wine and other alcohol consumption and risk of ovarian cancer in the California Teachers Study cohort CANCER CAUSES & CONTROL Chang, E. T., Canchola, A. J., Lee, V. S., Clarke, C. A., Purdie, D. M., Reynolds, P., Bernstein, L., Stram, D. O., Anton-Culver, H., Deapen, D., Mohrenweiser, H., Peel, D., Pinder, R., Ross, R. K., West, D. W., Wright, W., Ziogas, A., Horn-Ross, P. L. 2007; 18 (1): 91-103

    Abstract

    Whether alcohol consumption influences ovarian cancer risk is unclear. Therefore, we investigated the association between alcohol intake at various ages and risk of ovarian cancer.Among 90,371 eligible members of the California Teachers Study cohort who completed a baseline alcohol assessment in 1995-1996, 253 women were diagnosed with epithelial ovarian cancer by the end of 2003. Multivariate Cox proportional hazards regression analysis was performed to estimate relative risks (RRs) and 95% confidence intervals (CIs).Consumption of total alcohol, beer, or liquor in the year prior to baseline, at ages 30-35 years, or at ages 18-22 years was not associated with risk of ovarian cancer. Consumption of at least one glass per day of wine, compared to no wine, in the year before baseline was associated with increased risk of developing ovarian cancer: RR = 1.57 (95% CI 1.11-2.22), P (trend) = 0.01. The association with wine intake at baseline was particularly strong among peri-/post-menopausal women who used estrogen-only hormone therapy and women of high socioeconomic status.Alcohol intake does not appear to affect ovarian cancer risk. Constituents of wine other than alcohol or, more likely, unmeasured determinants of wine drinking were associated with increased risk of ovarian cancer.

    View details for DOI 10.1007/s10552-006-0083-x

    View details for Web of Science ID 000243031800009

    View details for PubMedID 17186425

  • Atopy and risk of non-Hodgkin lymphoma JOURNAL OF THE NATIONAL CANCER INSTITUTE Melbye, M., Smedby, K. E., Lehtinen, T., Rostgaard, K., Glimelius, B., Munksgaard, L., Schollkopf, C., Sundstrom, C., Chang, E. T., Koskela, P., Adami, H., Hjalgrim, H. 2007; 99 (2): 158-166

    Abstract

    A possible connection between allergy and cancer has been suspected, but allergy-related conditions or atopy have been inconsistently associated with reduced risks of non-Hodgkin lymphoma. We investigated this association in a population-based case-control study and in a prospective study with prediagnostic blood specimens.We carried out a population-based study of 3055 case patients with non-Hodgkin lymphoma and 3187 control subjects in Denmark and Sweden, including questionnaire information on allergy and blood specimens, and a nested case-control study within a prospective cohort of more than 400,000 Finnish women. In the second study, serum specimens from the 198 case patients who developed non-Hodgkin lymphoma within a median of 8.9 years after the blood was drawn were matched with serum specimens from 594 control subjects. In both studies, laboratory-based evidence of allergy (atopy) was determined in serum on the basis of specific IgE reactivity to common inhalant allergens. Dissemination of disease was classified by the Ann Arbor system. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by logistic regression.In the first study, ever having hay fever, but not other allergic conditions, was associated with a reduced risk of non-Hodgkin lymphoma. In particular, subjects with specific IgE reactivity in serum had a 32% (95% CI = 20% to 42%) lower risk of overall non-Hodgkin lymphoma than those without such reactivity. However, among case patients, dissemination of the disease was strongly inversely associated with specific IgE reactivity. In the second (i.e., prospective) study, no association was found between non-Hodgkin lymphoma and specific IgE reactivity, except possibly immediately before a diagnosis of non-Hodgkin lymphoma (> or = 10 years before diagnosis, OR = 1.00, 95% CI = 0.48 to 2.09; 5-9 years before, OR = 0.95, 95% CI = 0.50 to 1.84; 1-4 years before, OR = 0.33, 95% CI = 0.11 to 1.02; and < 1 year before, OR = 0.27, 95% CI = 0.03 to 2.31).Allergy may not be causally associated with the risk of non-Hodgkin lymphoma. The inverse association observed in some case-control studies may arise because non-Hodgkin lymphoma suppresses the immunologic response to allergens.

    View details for DOI 10.1093/inci/djk019

    View details for Web of Science ID 000243528300012

    View details for PubMedID 17227999

  • Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism INTERNATIONAL JOURNAL OF CANCER Hedelin, M., Chang, E. T., Wiklund, F., Bellocco, R., Klint, A., Adolfsson, J., Shahedi, K., Xu, J., Adami, H., Gronberg, H., Balter, K. A. 2007; 120 (2): 398-405

    Abstract

    Dietary intake of marine fatty acids from fish may protect against prostate cancer development. We studied this association and whether it is modified by genetic variation in cyclooxygenase (COX)-2, a key enzyme in fatty acid metabolism and inflammation. We assessed dietary intake of fish among 1,499 incident prostate cancer cases and 1,130 population controls in Sweden. Five single nucleotide polymorphisms (SNPs) were identified and genotyped in available blood samples for 1,378 cases and 782 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by multivariate logistic regression. Multiplicative and additive interactions between fish intake and COX-2 SNPs on prostate cancer risk were evaluated. Eating fatty fish (e.g., salmon-type fish) once or more per week, compared to never, was associated with reduced risk of prostate cancer (OR: 0.57, 95% CI: 0.43-0.76). The OR comparing the highest to the lowest quartile of marine fatty acids intake was 0.70 (95% CI: 0.51-0.97). We found a significant interaction (p < 0.001) between salmon-type fish intake and a SNP in the COX-2 gene (rs5275: +6365 T/C), but not with the 4 other SNPs examined. We found strong inverse associations with increasing intake of salmon-type fish among carriers of the variant allele (OR for once per week or more vs. never = 0.28, 95% CI: 0.18-0.45; p(trend) < 0.01), but no association among carriers of the more common allele. Frequent consumption of fatty fish and marine fatty acids appears to reduce the risk of prostate cancer, and this association is modified by genetic variation in the COX-2 gene.

    View details for DOI 10.1002/ijc.22319

    View details for Web of Science ID 000242868800025

    View details for PubMedID 17066444

  • Recent changes in breast cancer incidence and risk factor prevalence in San Francisco Bay area and California women: 1988 to 2004 BREAST CANCER RESEARCH Keegan, T. H., Chang, E. T., John, E. M., Horn-Ross, P. L., Wrensch, M. R., Glaser, S. L., Clarke, C. A. 2007; 9 (5)

    Abstract

    Historically, the incidence rate of breast cancer among non-Hispanic white women living in the San Francisco Bay area (SFBA) of California has been among the highest in the world. Substantial declines in breast cancer incidence rates have been documented in the United States and elsewhere during recent years. In light of these reports, we examined recent changes in breast cancer incidence and risk factor prevalence among non-Hispanic white women in the SFBA and other regions of California.Annual age-adjusted breast cancer incidence and mortality rates (1988 to 2004) were obtained from the California Cancer Registry and analyzed using Joinpoint regression. Population-based risk factor prevalences were calculated using two data sources: control subjects from four case-control studies (1989 to 1999) and the 2001 and 2003 California Health Interview Surveys.In the SFBA, incidence rates of invasive breast cancer increased 1.3% per year (95% confidence interval [CI], 0.7% to 2.0%) in 1988-1999 and decreased 3.6% per year (95% CI, 1.6% to 5.6%) in 1999-2004. In other regions of California, incidence rates of invasive breast cancer increased 0.8% per year (95% CI, 0.4% to 1.1%) in 1988-2001 and decreased 4.4% per year (95% CI, 1.4% to 7.3%) in 2001-2004. In both regions, recent (2000-2001 to 2003-2004) decreases in invasive breast cancer occurred only in women 40 years old or older and in women with all histologic subtypes and tumor sizes, hormone receptor-defined types, and all stages except distant disease. Mortality rates declined 2.2% per year (95% CI, 1.8% to 2.6%) from 1988 to 2004 in the SFBA and the rest of California. Use of estrogen-progestin hormone therapy decreased significantly from 2001 to 2003 in both regions. In 2003-2004, invasive breast cancer incidence remained higher (4.2%) in the SFBA than in the rest of California, consistent with the higher distributions of many established risk factors, including advanced education, nulliparity, late age at first birth, and alcohol consumption.Ongoing surveillance of breast cancer occurrence patterns in this high-risk population informs breast cancer etiology through comparison of trends with lower-risk populations and by highlighting the importance of examining how broad migration patterns influence the geographic distribution of risk factors.

    View details for DOI 10.1186/bcr1768

    View details for Web of Science ID 000253285800011

    View details for PubMedID 20210979

  • Hepatitis B and liver cancer knowledge and preventive practices among Asian Americans in the San Francisco Bay Area, California ASIAN PACIFIC JOURNAL OF CANCER PREVENTION Wu, C. A., Lin, S. Y., So, S. K., Chang, E. T. 2007; 8 (1): 127-134

    Abstract

    Chronic hepatitis B virus (HBV) infection causes liver cancer and disproportionately affects the Asian community in the U.S. In order to advance HBV and liver cancer awareness and prevention, it is important to identify existing gaps in knowledge and preventive practices among Asian Americans. Therefore, the authors administered a written questionnaire to 199 adults in the Asian-American community of the San Francisco Bay Area, California. Although the majority of adults had at least a college education, knowledge regarding HBV transmission, prevention, symptoms, risks, and occurrence was low. Fewer than 60% reported having been tested for HBV, only 31% reported having been vaccinated against HBV, and only 44% reported having had their children vaccinated. Asians, especially those born in China or Southeast Asia, had significantly poorer knowledge regarding HBV and liver cancer than non-Asians. Those with higher knowledge levels were significantly more likely to have been tested for HBV and to have had their children vaccinated. Younger adults, women, Caucasians, more highly educated individuals, those not born in China or Hong Kong, and those with a personal or family history of liver disease were more likely to have taken preventive action against HBV. Our results suggest that HBV and liver cancer knowledge among Asian Americans, especially Chinese Americans, is poor, and that better knowledge is associated with increased preventive practices. Thus, there is a need for increased HBV education and improved community-based interventions to prevent HBV-related liver disease in the high-risk Asian-American community.

    View details for Web of Science ID 000253887000026

    View details for PubMedID 17477787

  • The non-Hodgkin lymphomas: A review of the epidemiologic literature INTERNATIONAL JOURNAL OF CANCER Alexander, D. D., Mink, P. J., Adami, H., Chang, E. T., Cole, P., Mandel, J. S., Trichopoulos, D. 2007: 1-39

    Abstract

    The non-Hodgkin lymphomas (NHL) are a heterogeneous group of B-cell and T-cell neoplasms that arise primarily in the lymph nodes. NHL incidence rates in the US doubled between about 1970 and 1990, and stabilized during the 1990s. NHL accounts for approximately 3.4% of cancer deaths in the US. Although some of the observed patterns in NHL have been related to HIV/AIDS, these conditions cannot fully explain the magnitude of the changes; neither do changes in classification systems nor improved diagnostic capabilities. Studies of occupational and environmental exposures (e.g., pesticides, solvents) have produced no consistent pattern of significant positive associations. Inverse associations with ultraviolet radiation exposure and alcohol and fish intake, and positive associations with meat and saturated fat intake have been reported in several studies; additional studies are needed to confirm or refute these associations. Family history of NHL or other hematolympho-proliferative cancers and personal history of several autoimmune disorders are associated with increased risk of NHL, but are not likely to account for a large proportion of cases. HIV and other infectious agents, such as human herpesvirus 8 and Epstein-Barr, appear to be associated with differing types of NHL, such as some B-cell lymphomas. Future epidemiologic studies should evaluate associations by NHL type, enhance exposure information collected, and elucidate factors that may identify susceptible (or resistant) subpopulations because of genetic, immunologic or other characteristics. The extent to which the etiology of NHL types may differ is important to resolve in ongoing and future studies.

    View details for DOI 10.1002/ijc.22719

    View details for Web of Science ID 000245959100001

    View details for PubMedID 17405121

  • Recent breast cancer trends among Asian/Pacific Islander, Hispanic, and African-American women in the US: changes by tumor subtype BREAST CANCER RESEARCH Hausauer, A. K., Keegan, T. H., Chang, E. T., Clarke, C. A. 2007; 9 (6)

    Abstract

    Recently, unprecedented drops in breast cancer incidence have been reported for populations of mostly White European descent. Incidence patterns in non-White racial/ethnic groups are less described. Therefore, we examined population-based breast cancer incidence trends separately for US Asian/Pacific Islander, Hispanic, African-American, and non-Hispanic White women by etiologically relevant tumor subtype characteristics, including hormone receptor status, histology, size, and in situ behavior.We obtained breast cancer data from 13 Surveillance, Epidemiology, and End Results (SEER) cancer registries to calculate age-adjusted incidence rates and trends, stratified by race/ethnicity and tumor subtype for the period 1992-2004. Detailed analyses were limited to women 50 years old or older. Joinpoint regression was used to assess incidence trends by annual quarter of diagnosis.Between 2001 and 2004, incidence rates of invasive breast cancer in women 50 years old or older declined appreciably among Asians/Pacific Islanders (-8.5%) and Hispanics (-2.9%) and were stable in African-Americans (+0.5%), reductions substantially lower than those observed among non-Hispanic Whites (-14.3%). In Asian/Pacific Islander women, perceptible but statistically nonsignificant decreases were observed for hormone receptor-positive, lobular, and small tumors only. Rates of hormone receptor-negative tumors increased among African-Americans (26.1%) and Hispanics (26.9%) during 2001-2004. Incidence trends in most groups, except African-American women, peaked between 1999 and mid-2002. Rates of in situ cancer remained stable in all groups.Recently reported reductions in breast cancer incidence varied considerably by race/ethnicity. These patterns are consistent with documented racial/ethnic differences in the prevalence and discontinuation of hormone therapy (HT) after July 2002 but do not correspond as well to patterns of mammography use in these groups. The data presented in this analysis provide further evidence that population-level HT use is a major influence on population-level rates of particular breast cancer subtypes, especially receptor-positive tumors.

    View details for DOI 10.1186/bcr1839

    View details for Web of Science ID 000253285900027

    View details for PubMedID 18162138

  • Understanding the validity of self-reported positive family history of lymphoma in extended families to facilitate genetic epidemiology and clinical practice LEUKEMIA & LYMPHOMA Glaser, S. L., Chang, E. T., Horning, S. J., Clarke, C. A. 2007; 48 (6): 1110-1118

    Abstract

    The validity of self-reported information about familial Hodgkin lymphoma (HL), important for epidemiologic research and clinical practice, is undetermined. We attempted to validate 55 familial lymphomas previously reported by 48 subjects in a population-based case-control study of HL in women. Of 44 diagnoses (80%) reported by 40 (83%) recontacted subjects, we obtained medical documentation for 36 (82%). Twenty-nine (81%) were validated as lymphoma, with accuracy better for first-degree relatives and subjects with larger nuclear families and other family illness. Fourteen reports of familial HL were validated as lymphoma for 13 (93%) and as HL for nine (64%). Fifteen reports of familial NHL were validated as lymphoma for 10 (67%) and as NHL for 10 (67%). Thus, familial HL reported by HL patients and controls is highly likely to be lymphoma even in extended family members but less likely to be HL per se. Validity may vary with the subject's family size and medical history.

    View details for DOI 10.1080/10428190701302434

    View details for Web of Science ID 000247779100012

    View details for PubMedID 17577774

  • Nutrient intake and risk of non-Hodgkin's lymphoma AMERICAN JOURNAL OF EPIDEMIOLOGY Chang, E. T., Balter, K. M., Torrang, A., Smedby, K. E., Melbye, M., Sundstrom, C., Glimelius, B., Adami, H. 2006; 164 (12): 1222-1232

    Abstract

    The mechanisms through which diet may influence the development of non-Hodgkin's lymphoma (NHL) are unclear but can be better understood by examining associations between nutrient consumption and NHL risk. Between 2000 and 2002, 591 NHL cases and 460 population-based controls in Sweden completed a semiquantitative food frequency questionnaire. Unconditional logistic regression was performed to estimate odds ratios and 95% confidence intervals for associations with nutrient intake; all statistical tests were two sided. Dietary intake of most macronutrients was not associated with risk of NHL or its common subtypes. Consumption of omega-3 or marine fatty acids was associated with decreased risk of NHL and chronic lymphocytic lymphoma, and dietary fiber was associated with lower risk of all subtypes examined. When the highest and the lowest quartiles of marine fat intake were compared, the odds ratio for NHL risk was 0.6 (95% confidence interval: 0.4, 0.9), ptrend=0.03; for dietary fiber intake, the corresponding odds ratio was 0.5 (95% confidence interval: 0.3, 0.7), ptrend<0.001. Dietary consumption of beta-carotene or alpha-tocopherol was associated with lower NHL risk, whereas intake of calcium or retinol was associated with increased NHL risk. Nutrients that affect inflammation, vitamin D activity, oxidative DNA damage, or DNA methylation may be associated with risk of NHL.

    View details for DOI 10.1093/aje/kwj330

    View details for Web of Science ID 000242714800010

    View details for PubMedID 17005624

  • Dietary intake of phytoestrogens, estrogen receptor-beta polymorphisms and the risk of prostate cancer PROSTATE Hedelin, M., Balter, K. A., Chang, E. T., Bellocco, R., Klint, A., Johansson, J., Wiklund, F., Thellenberg-Karlsson, C., Adami, H., Gronberg, H. 2006; 66 (14): 1512-1520

    Abstract

    The causes of prostate cancer are poorly understood, but genetic factors may be more important than for many other malignancies, and dietary phytoestrogens may be protective. Because phytoestrogens bind tightly to the estrogen receptor-beta, we conducted an epidemiologic investigation of synergistic effects between phytoestrogen intake and estrogen receptor-beta gene polymorphisms.We performed a population-based case-control study in Sweden. All participants reported their phytoestrogen intake and donated a blood sample. We identified four haplotype-tagging single nucleotide polymorphisms (htSNPs) and genotyped these htSNPs in 1314 prostate cancer patients and 782 controls. Odds ratios were estimated by multivariate logistic regression. Interactions between phytoestrogen intake and estrogen receptor-beta SNPs on prostate cancer risk were evaluated considering both multiplicative and additive effect scales.We found a significant multiplicative interaction (P = 0.04) between dietary intake of phytoestrogens and a promoter SNP in the estrogen receptor-beta gene (rs 2987983-13950), but not with any of the three other htSNPs (P = 0.11, 0.69, 0.85). Among carriers of the variant promoter alleles, we found strong inverse associations with increasing intake of total phytoestrogens (odds ratio for highest vs. lowest quartile = 0.43; P for trend <0.001), isoflavonoids (odds ratio = 0.63; P for trend = 0.05), and coumestrol (odds ratio = 0.57; P for trend = 0.003). We found no association between phytoestrogens and prostate cancer among carriers homozygous for the wild-type allele (TT).Our study provides strong evidence that high intake of phytoestrogens substantially reduce prostate cancer risk among men with specific polymorphic variation in the promoter region of the estrogen receptor-beta gene.

    View details for DOI 10.1002/pros.20487

    View details for Web of Science ID 000240707700005

    View details for PubMedID 16921512

  • The enigmatic epidemiology of nasopharyngeal carcinoma CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Adami, H. 2006; 15 (10): 1765-1777

    Abstract

    Nasopharyngeal carcinoma (NPC) has a unique and complex etiology that is not completely understood. Although NPC is rare in most populations, it is a leading form of cancer in a few well-defined populations, including natives of southern China, Southeast Asia, the Arctic, and the Middle East/North Africa. The distinctive racial/ethnic and geographic distribution of NPC worldwide suggests that both environmental factors and genetic traits contribute to its development. This review aims to summarize the current knowledge regarding the epidemiology of NPC and to propose new avenues of research that could help illuminate the causes and ultimately the prevention of this remarkable disease. Well-established risk factors for NPC include elevated antibody titers against the Epstein-Barr virus, consumption of salt-preserved fish, a family history of NPC, and certain human leukocyte antigen class I genotypes. Consumption of other preserved foods, tobacco smoking, and a history of chronic respiratory tract conditions may be associated with elevated NPC risk, whereas consumption of fresh fruits and vegetables and other human leukocyte antigen genotypes may be associated with decreased risk. Evidence for a causal role of various inhalants, herbal medicines, and occupational exposures is inconsistent. Other than dietary modification, no concrete preventive measures for NPC exist. Given the unresolved gaps in understanding of NPC, there is a clear need for large-scale, population-based molecular epidemiologic studies to elucidate how environmental, viral, and genetic factors interact in both the development and the prevention of this disease.

    View details for DOI 10.1158/1055-9965.EPI-06-0353

    View details for Web of Science ID 000241616800005

    View details for PubMedID 17035381

  • Cancer risk among patients with condylomata acuminata INTERNATIONAL JOURNAL OF CANCER Nordenvall, C., Chang, E. T., Adami, H., Ye, W. 2006; 119 (4): 888-893

    Abstract

    Condylomata acuminata have been shown to increase the risk of anogenital cancers. However, previous studies have been of limited sample size and/or short follow-up duration, which prevent precise estimates of long-term excess risk, especially for specific cancer sites. We estimated the risk of specific cancers in a large cohort of hospitalized patients with condylomata acuminata, as recorded in the Swedish Inpatient Register between 1965 and 1999. Altogether, 10,971 patients (1,685 men and 9,286 women) were followed through 1999 for a median of 13 years. The standardized incidence ratio (SIR)--the ratio of the observed number of cancers to the number expected on the basis of the incidence in the Swedish population at large--was used as a measure of relative risk. After excluding the first-year of follow-up, we observed 43 cases of anogenital cancer in women, and 7 cases in men. Risks were elevated for cancers of the vulva (N = 13, SIR = 10.2, 95% confidence interval (CI) = 5.4-17.4), vagina (N = 4, SIR = 12.0, 95% CI = 3.3-30.7) and penis (N = 5, SIR = 21.9, 95% CI = 7.1-51.2). There was a moderate excess risk of cervical cancer in situ (N = 259, SIR = 1.9, 95% CI = 1.7-2.1), but not invasive cervical cancer. Excess risks of esophageal, buccal cavity, nonmelanoma skin, lung and bladder cancers, and Hodgkin and non-Hodgkin lymphoma, were also observed in both men and women. In conclusion, condylomata acuminata are strongly associated with increased risk of cancers of the vulva, vagina, penis and anus, as well as some nonanogenital malignancies, but not invasive cervical cancer.

    View details for DOI 10.1002/ijc.21892

    View details for Web of Science ID 000238988800023

    View details for PubMedID 16557590

  • Body size, physical activity, and risk of Hodgkin's lymphoma in women CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Keegan, T. H., Glaser, S. L., Clarke, C. A., Dorfman, R. F., Mann, R. B., DiGiuseppe, J. A., Chang, E. T., Ambinder, R. F. 2006; 15 (6): 1095-1101

    Abstract

    Few studies have examined the associations of body size and physical activity with the development of Hodgkin's lymphoma (HL) in women. In data from a population-based case-control study in women ages 19 to 79 years, we assessed the relation of self-report height, weight, body mass index (BMI), and strenuous physical activity to HL risk in 312 cases with diagnostic re-review and 325 random-digit dialed controls using logistic regression. Analyses were stratified by age group and tumor cell presence of EBV. After adjustment for social class measures, taller childhood and adult height were associated with higher HL risk. In women ages 19 to 44 years, HL risk was elevated for higher, but healthy, BMI values, whereas in women ages 45 to 79 years, associations with BMI were inverse. The odds of developing HL were lower with participation (versus nonparticipation) in strenuous physical activity in the past year [odds ratio (OR), 0.58; 95% confidence interval (95% CI), 0.39-0.87 in women 19-44 years; OR, 0.45; 95% CI, 0.19-1.06 in women 45-79 years] and throughout adult life, and with sports team membership (versus nonmembership) in high school and/or at ages 18 to 22 years. Results were similar in cases (n = 269) with and without tumor-cell EBV compared with controls, although the inverse association with physical activity was somewhat stronger for women with EBV-positive disease. These findings show that in women, body size and strenuous physical activity, both modifiable characteristics, are associated with HL risk in adult life possibly through immunologic, infectious, or genetic mechanisms.

    View details for DOI 10.1158/1055-9965.EPI-06-0020

    View details for Web of Science ID 000238300100007

    View details for PubMedID 16775165

  • Dietary phytoestrogen, serum enterolactone and risk of prostate cancer: the Cancer Prostate Sweden Study (Sweden) CANCER CAUSES & CONTROL Hedelin, M., Klint, A., Chang, E. T., Bellocco, R., Johansson, J. E., Andersson, S. O., Heinonen, S. M., ADLERCREUTZ, H., Adami, H. O., Gronberg, H., Balter, K. A. 2006; 17 (2): 169-180

    Abstract

    Based on evidence that phytoestrogens may protect against prostate cancer, we evaluated the associations between serum enterolactone concentration or dietary phytoestrogen intake and risk of prostate cancer.In our Swedish population-based case-control study, questionnaire-data were available for 1,499 prostate cancer cases and 1,130 controls, with serum enterolactone levels in a sub-group of 209 cases and 214 controls. Unconditional logistic regression was performed to estimate multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with risk of prostate cancer.High intake of food items rich in phytoestrogens was associated with a decreased risk of prostate cancer. The OR comparing the highest to the lowest quartile of intake was 0.74 (95% CI: 0.57-0.95; p-value for trend: 0.01). In contrast, we found no association between dietary intake of total or individual lignans or isoflavonoids and risk of prostate cancer. Intermediate serum levels of enterolactone were associated with a decreased risk of prostate cancer. The ORs comparing increasing quartiles of serum enterolactone concentration to the lowest quartile were, respectively, 0.28 (95% CI: 0.15-0.55), 0.63 (95% CI: 0.35-1.14) and 0.74 (95% CI: 0.41-1.32).Our results support the hypothesis that certain foods high in phytoestrogens are associated with a lower risk of prostate cancer.

    View details for DOI 10.1007/s10552-005-0342-2

    View details for Web of Science ID 000234754500006

    View details for PubMedID 16425095

  • Variation in DNA repair genes ERCC2, XRCC1, and XRCC3 and risk of follicular lymphoma CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Smedby, K. E., Lindgren, C. M., Hjalgrim, H., Humphreys, K., Schollkopf, C., Chang, E. T., Roos, G., Ryder, L. P., Falk, K. I., Palmgren, J., Kere, J., Melbye, M., Glimelius, B., Adami, H. O. 2006; 15 (2): 258-265

    Abstract

    The reasons for the positive association between skin cancer and non-Hodgkin's lymphoma are not known but may be due to common susceptibility involving suboptimal DNA repair. Therefore, we investigated selected polymorphisms and haplotypes in three DNA repair genes, previously associated with skin cancer and DNA repair capacity, in risk of follicular lymphoma, including possible gene interaction with cigarette smoking and sun exposure. We genotyped 19 single nucleotide polymorphisms (SNP) in the ERCC2, XRCC1, and XRCC3 genes in 430 follicular lymphoma patients and 605 controls within a population-based case-control study in Denmark and Sweden. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression and haplotype associations were assessed with a global score test. We observed no associations between variation in the ERCC2 and XRCC1 genes and follicular lymphoma risk. In XRCC3, increased risk of follicular lymphoma was suggested for rare homozygotes of three SNPs [Rs3212024: OR, 1.8 (95% CI, 1.1-2.8); Rs3212038: OR, 1.5 (95% CI, 1.0-2.4); Rs3212090: OR, 1.5 (95% CI, 1.0-2.5)]. These results were strengthened in current cigarette smokers. However, evidence of differences in XRCC3 haplotype distributions between follicular lymphoma cases and controls was weak, both overall and in current smokers. We conclude that polymorphic variation in the XRCC3 gene, but not in ERCC2 or XRCC1, may be of importance for susceptibility to follicular lymphoma, perhaps primarily in current smokers. The link between skin cancer and follicular lymphoma is unlikely to be mediated through common variation in the studied DNA repair gene polymorphisms.

    View details for DOI 10.1158/1055-9965.EPI-05-0583

    View details for Web of Science ID 000235587200010

    View details for PubMedID 16492913

  • Autoimmune and chronic inflammatory disorders and risk of non-Hodgkin lymphoma by subtype JOURNAL OF THE NATIONAL CANCER INSTITUTE Smedby, K. E., Hjalgrim, H., Askling, J., T Chang, E., Gregersen, H., Porwit-MacDonald, A., SUNDSTROM, C., Akerman, M., Melbye, M., Glimelius, B., Adami, H. O. 2006; 98 (1): 51-60

    Abstract

    Some autoimmune and chronic inflammatory disorders are associated with increased risks of non-Hodgkin lymphoma (NHL). Because different NHL subtypes develop at different stages of lymphocyte differentiation, associations of autoimmune and inflammatory disorders with specific NHL subtypes could lead to a better understanding of lymphomagenic mechanisms.In a population-based case-control study in Denmark and Sweden, 3055 NHL patients and 3187 matched control subjects were asked about their history of autoimmune and chronic inflammatory disorders, markers of severity, and treatment. Logistic regression with adjustment for study matching factors was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for NHL overall and for NHL subtypes.Risks of all NHL were increased in association with rheumatoid arthritis (OR = 1.5, 95% CI = 1.1 to 1.9), primary Sjögren syndrome (OR = 6.1, 95% CI = 1.4 to 27), systemic lupus erythematosus (OR = 4.6, 95% CI = 1.0 to 22), and celiac disease (OR = 2.1, 95% CI = 1.0 to 4.8). All of these conditions were also associated with diffuse large B-cell lymphoma, and some were associated with marginal zone, lymphoplasmacytic, or T-cell lymphoma. Ever use of nonsteroidal anti-inflammatory drugs, systemic corticosteroids, and selected immunosuppressants was associated with risk of NHL in rheumatoid arthritis patients but not in subjects without rheumatoid arthritis. Also, multivariable adjustment for treatment had little impact on risk estimates. Psoriasis, sarcoidosis, and inflammatory bowel disorders were not associated with increased risk of NHL overall or of any NHL subtype.Our results confirm the associations between certain autoimmune disorders and risk of NHL and suggest that the associations may not be general but rather mediated through specific NHL subtypes. These NHL subtypes develop during postantigen exposure stages of lymphocyte differentiation, consistent with a role of antigenic drive in autoimmunity-related lymphomagenesis.

    View details for DOI 10.1093/jnci/dj004

    View details for Web of Science ID 000234715800010

    View details for PubMedID 16391371

  • Reliability of self-reported family history of cancer in a large case-control study of lymphoma JOURNAL OF THE NATIONAL CANCER INSTITUTE Chang, E. T., Smedby, K. E., Hjalgrim, H., Glimelius, B., Adami, H. O. 2006; 98 (1): 61-68

    Abstract

    Case-control studies of familial cancer risk traditionally rely on self-reported family history of cancer, which may bias results due to differential recall between case patients and control subjects. To evaluate the reliability of self-reported data, we analyzed questionnaire and registry-based data on familial cancer from a population-based case-control study of malignant lymphoma.All 1508 lymphoma case patients and 1229 control subjects completed a telephone interview assessing cancer in family members. Participants were linked to the Swedish Multi-Generation Register and Cancer Register to identify confirmed cancer diagnoses in first-degree relatives. The sensitivity and specificity of self-reported familial cancer were calculated among case patients and control subjects and were compared using logistic regression. All statistical tests were two-sided.Lymphoma case patients reported a family history of any cancer with statistically significantly higher sensitivity than control subjects (0.85, 95% confidence interval [CI] = 0.83 to 0.87 and 0.80, 95% CI = 0.77 to 0.82, respectively) but with marginally lower specificity (0.89, 95% CI = 0.87 to 0.91 and 0.92, 95% CI = 0.90 to 0.94, respectively). The sensitivity of self-reporting familial cancers by site ranged from less than 0.20 for rare malignancies to nearly 0.75 for more common types, whereas specificity was generally 0.98 or greater. For most sites, the reliability of self-report was similar in patients and control subjects. However, patients reported familial hematopoietic cancer with statistically significantly higher sensitivity (0.60, 95% CI = 0.57 to 0.62) than control subjects (0.38, 95% CI = 0.35 to 0.40). Odds ratios for the association between familial cancer and risk of non-Hodgkin lymphoma were consistently higher when based on self-reported, compared with registry data-based, family history of any cancer or of hematopoietic cancer.Reliability of self-reported family history of cancer varies between case patients and control subjects. Recall bias may thus produce biased results in case-control studies of familial cancer risk.

    View details for DOI 10.1093/jnci/djj005

    View details for Web of Science ID 000234715800011

    View details for PubMedID 16391372

  • Medication use and risk of non-Hodgkin's lymphoma AMERICAN JOURNAL OF EPIDEMIOLOGY Chang, E. T., Smedby, K. E., Hjalgrim, H., Schollkopf, C., Porwit-MacDonald, A., SUNDSTROM, C., Tani, E., d'Amore, F., Melbye, M., Adami, H. O., Glimelius, B. 2005; 162 (10): 965-974

    Abstract

    Conflicting results from previous epidemiologic studies shed little light on whether medication use is associated with risk of non-Hodgkin's lymphoma (NHL). To investigate this question, the authors conducted a population-based case-control study in Denmark and Sweden from 1999 to 2002, including 3,055 incident NHL cases and 3,187 controls. Participants reported their past use of medications and history of particular medical conditions. Unconditional logistic regression was used to estimate multivariate odds ratios and 95% confidence intervals for the associations between medication use and risk of NHL; all statistical tests were two sided. Use of antibiotics more than 10 times during adulthood was positively associated with risk of NHL and most major NHL subtypes; when users were compared with nonusers, the odds ratio for NHL was 1.8 (95% confidence interval: 1.4, 2.3); p(trend) for total antibiotic use <0.001. In addition, high cumulative use of nonsteroidal anti-inflammatory drugs was marginally associated with elevated NHL risk. Other medications evaluated were not associated with risk of NHL or its most common subtypes. Findings suggest that inflammation, infections, susceptibility to infections, and/or use of antibiotics or nonsteroidal anti-inflammatory drugs to treat these conditions may increase the risk of NHL. However, most of the medications examined were not associated with NHL risk.

    View details for DOI 10.1093/aje/kwi311

    View details for Web of Science ID 000233218800004

    View details for PubMedID 16192343

  • Family history of hematopoietic malignancy and risk of lymphoma JOURNAL OF THE NATIONAL CANCER INSTITUTE Chang, E. T., Smedby, K. E., Hjalgrim, H., Porwit-MacDonald, A., Roos, G., Glimelius, B., Adami, H. O. 2005; 97 (19): 1466-1474

    Abstract

    A family history of hematopoietic malignancy is associated with an increased risk of non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL), although the magnitude of the relative risk is unclear. We estimated the association between familial hematopoietic cancer and risk of lymphoma using validated, registry-based family data, and we also investigated whether associations between some environmental exposures and risk of lymphoma vary between individuals with and without such a family history.In a population-based case-control study of malignant lymphoma, 1506 case patients and 1229 control subjects were linked to the Swedish Multi-Generation Register and then to the Swedish Cancer Register to ascertain history of cancer in first-degree relatives of patients with malignant lymphoma. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with the risk of lymphoma.A history of hematopoietic malignancy in any first-degree relative was associated with an increased risk of all NHL (OR = 1.8, 95% CI = 1.2 to 2.5), common B-cell NHL subtypes, and HL. Relative risks were generally stronger in association with sibling hematopoietic cancer (OR for all NHL = 3.2, 95% CI = 1.3 to 7.6) than with parental hematopoietic cancer (OR = 1.6, 95% CI = 1.1 to 2.3). A family history of NHL or chronic lymphocytic leukemia (CLL) was associated with an increased risk of several NHL subtypes and HL, whereas familial multiple myeloma was associated with a higher risk of follicular lymphoma. There was no statistically significant heterogeneity in NHL risk associations with environmental factors between individuals with and without familial hematopoietic malignancy.The increased risk of NHL and HL among individuals with a family history of hematopoietic malignancy was approximately twofold for both lymphoma types. There was no evidence that etiologic associations varied between familial NHL and nonfamilial NHL.

    View details for DOI 10.1093/jnci/dji293

    View details for Web of Science ID 000232953400013

    View details for PubMedID 16204696

  • Alcohol consumption and risk of non-Hodgkin lymphoma: a pooled analysis LANCET ONCOLOGY Morton, L. M., Zheng, T. Z., Holford, T. R., Holly, E. A., Chiu, B. C., Costantini, A. S., Stagnaro, E., Willett, E. V., Dal Maso, L., Serraino, D., Chang, E. T., Cozen, W., Davis, S., Severson, R. K., Bernstein, L., Mayne, S. T., Dee, F. R., Cerhan, J. R., Hartge, P. 2005; 6 (7): 469-476

    Abstract

    Previous epidemiological studies of the relation between alcohol consumption and risk of non-Hodgkin lymphoma (NHL) have been inconsistent, probably because of small sample sizes of individual studies that result from stratification by NHL subtype and type of alcoholic beverage. We aimed to assess the role of alcohol consumption in NHL with sufficient sample size to analyse by both type of alcoholic beverage and disease subtype.We obtained original data from nine case-control studies from the USA, UK, Sweden, and Italy in the International Lymphoma Epidemiology Consortium (InterLymph), yielding a pooled study population of 15 175 individuals (6492 cases and 8683 controls). We derived odds ratios (OR) and 95% CI from unconditional logistic regression models, controlling for study centre and other confounding factors. Heterogeneity between studies was assessed by comparison of results from joint fixed-effects logistic regression and two-stage random-effects logistic regression, and by calculation of Wald chi(2) statistics.People who drank alcohol had a lower risk of NHL than did non-drinkers (OR 0.83 [95% CI 0.76-0.89]). Compared with non-drinkers, risk estimates were lower for current drinkers than for former drinkers (0.73 [0.64-0.84] vs 0.95 [0.80-1.14]), but risk did not decrease with increasing alcohol consumption. The protective effect of alcohol did not vary by beverage type, but did change with NHL subtype. The lowest risk estimates were recorded for Burkitt's lymphoma (0.51 [0.33-0.77]).People who drink alcoholic beverages might have a lower risk of NHL than those who do not, and this risk might vary by NHL subtype. Further study designs are needed to determine whether confounding lifestyle factors or immunomodulatory effects of alcohol explain this association.

    View details for DOI 10.1016/S1470-2045(05)70214-X

    View details for Web of Science ID 000230367100016

    View details for PubMedID 15992695

  • Seasonal variation in the diagnosis of Hodgkin lymphoma in Sweden INTERNATIONAL JOURNAL OF CANCER Chang, E. T., Blomqvist, P., Lambe, M. 2005; 115 (1): 127-130

    Abstract

    Epidemiologic evidence suggests a seasonal pattern in the occurrence of Hodgkin lymphoma (HL), with an incidence peak around the month of March. This pattern may reflect seasonal variation in the prevalence of an infectious agent involved in HL development. Using Poisson regression, we examined monthly variation in HL diagnosis in Sweden between 1958 and 1998, based on data from the population-based Swedish Cancer Registry. Older adults (50 to 79 years) were marginally more likely to be diagnosed in February, but there was no monthly variation after stratifying by sex. Young adult males (15 to 49 years) presented more often in February, whereas young adult females presented less often in August and December. Among children (<15 years), boys were significantly more likely to have been diagnosed in March, whereas there was no seasonal incidence pattern among girls. The seasonal pattern in HL diagnosis among young adults and boys is consistent with an infectious origin, whereas the results among older adults neither support nor dispute the possibility of an infectious etiology in this age group.

    View details for DOI 10.1002/ijc.20832

    View details for Web of Science ID 000228530600016

    View details for PubMedID 15660399

  • Alcohol drinking and risk of localized versus advanced and sporadic versus familial prostate cancer in Sweden CANCER CAUSES & CONTROL Chang, E. T., Hedelin, M., Adami, H. O., Gronberg, H., Balter, K. A. 2005; 16 (3): 275-284

    Abstract

    It is unknown whether the association of alcohol consumption with prostate cancer risk varies between localized and advanced cases, or between sporadic and familial cases.We assessed recent alcohol drinking in a population-based case--control study of Swedish men, including 1499 cases and 1130 controls. Drinking status and average volume, frequency, and type of alcohol consumed were evaluated. Unconditional logistic regression was performed to estimate the odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for associations between alcohol consumption and prostate cancer risk.Prostate cancer cases were more likely than controls to be current or former, rather than never, drinkers. However, there was no association between recent total alcohol, beer, wine, and liquor consumption and risk of overall prostate cancer, nor advanced, sporadic, or familial prostate cancer. The OR for risk of overall disease among men who drank more than 135 g of total alcohol per week versus non-drinkers was 1.2 (95% CI: 0.9, 1.5), p(trend)=0.12. There was a marginal positive association between alcohol intake and risk of localized disease.We detected no association between recent alcohol consumption and risk of advanced, sporadic, or familial prostate cancer, and a borderline positive association with localized disease.

    View details for DOI 10.1007/s10552-004-3364-2

    View details for Web of Science ID 000229736900009

    View details for PubMedID 15947879

  • Body mass index and risk of malignant lymphoma in Scandinavian men and women JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE Chang, E. T., Hjalgrim, H., Smedby, K. E., Akerman, M., Tani, E., Johnsen, H. E., Glimelius, B., Adami, H. O., Melbye, M. 2005; 97 (3): 210-218

    Abstract

    The incidence of non-Hodgkin lymphoma and prevalence of obesity are increasing globally. A suggested positive association between obesity and risk of non-Hodgkin lymphoma has prompted us to investigate the relationship between body mass index (BMI) and risk of malignant lymphoma subtypes in a population-based case-control study.Telephone interviews were conducted with 3055 case patients with non-Hodgkin lymphoma and 618 case patients with Hodgkin lymphoma diagnosed between October 1, 1999, and August 30, 2002, and 3187 population-based control subjects. The interviews assessed current height, normal adult weight, and other possible risk factors. Multivariable odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for risk of lymphoma were estimated by unconditional logistic regression. All statistical tests were two-sided.BMI was not associated with risk of overall non-Hodgkin lymphoma or of Hodgkin lymphoma (for example, comparing the highly obese group [BMI > or =35.0 kg/m2] with the normal-weight group [BMI = 18.5-24.9 kg/m2], OR for risk of non-Hodgkin lymphoma = 0.9, 95% CI = 0.6 to 1.3; P(trend) across all categories of BMI = .27). BMI was also not associated with risk of any non-Hodgkin lymphoma subtype evaluated, although there was some evidence of a positive association with risk of diffuse large B-cell lymphoma (for example, comparing the highly obese group with the normal-weight group, OR for diffuse large B-cell lymphoma = 1.5, 95% CI = 0.9 to 2.4; P(trend) =.05).Excess weight does not appear to be associated with an increased risk of malignant lymphoma in general, or with a risk of most major lymphoma subtypes. Hence, the growing incidence of obesity is unlikely to be an important contributor to the increasing incidence of non-Hodgkin lymphoma worldwide.

    View details for DOI 10.1093/jnci/dji012

    View details for Web of Science ID 000226748200012

    View details for PubMedID 15687364

  • Dietary factors and risk of non-Hodgkin lymphoma in men and women CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Smedby, K. E., Zhang, S. M., Hjalgrim, H., Melbye, M., Ost, A., Glimelius, B., Wolk, A., Adami, H. O. 2005; 14 (2): 512-520

    Abstract

    The incidence of non-Hodgkin lymphoma (NHL) has increased worldwide in recent decades. Diet could influence NHL risk by modulating the immune system, although evidence is limited. We did a population-based case-control study to determine whether differences in diet were associated with NHL risk.A total of 597 NHL cases and 467 population controls in Sweden completed a semiquantitative food frequency questionnaire evaluating their dietary habits 2 years before the interview. Unconditional logistic regression was used to estimate the odds ratios (OR) and corresponding 95% confidence intervals (95% CI) for associations between food intake and risk of NHL.High consumption of dairy products and fried red meat was associated with increased risk of NHL. The OR of NHL for individuals in the highest quartile compared with the lowest quartile of dairy intake was 1.5 (95% CI, 1.1-2.2; P(trend) = 0.003). The OR for the highest versus lowest quartile of fried red meat intake was 1.5 (95% CI, 1.0-2.1; P(trend) = 0.02). In contrast, high consumption of fruits and vegetables was associated with reduced risk of NHL, particularly follicular lymphoma, among women but not men. Compared with the lowest quartile of vegetable intake, the OR of follicular lymphoma among women in the highest quartile of vegetable intake was 0.3 (95% CI, 0.1-0.7; P(trend) = 0.002).The positive associations of NHL risk with dairy products and fried red meat and the inverse association with fruits and vegetables suggest that diet affects NHL risk and could explain the increase of some histopathogic subtypes.

    View details for Web of Science ID 000227113800033

    View details for PubMedID 15734980

  • Alcohol intake and risk of non-Hodgkin lymphoma in men and women CANCER CAUSES & CONTROL Chang, E. T., Smedby, K. E., Zhang, S. M., Hjalgrim, H., Melbye, M., Ost, A., Wolk, A., Adami, H. O., Glimelius, B. 2004; 15 (10): 1067-1076

    Abstract

    The effect of alcohol intake on risk of NHL is unclear. We therefore conducted a population-based case-control study to examine the association between alcohol and NHL risk.613 NHL cases and 480 population controls in Sweden reported their average consumption of beer, wine, and liquor 2 years before the study. Unconditional logistic regression was used to estimate the odds ratios (OR) and corresponding 95% confidence intervals (CI) for associations between alcohol intake and NHL risk.Intake of total alcohol, beer, wine, or liquor was not associated with risk of overall NHL. There was no difference in risk of NHL among those who habitually consumed above 19.1 g of ethanol per day, compared to those who consumed on average 0-2.2 g of ethanol per day (OR = 1.2 (95% CI: 0.8, 1.7); Ptrend = 0.29). However, the association was significantly positive among males (OR = 1.8 (95% CI: 1.1, 2.9); Ptrend = 0.06). Total alcohol, beer, wine, or liquor intake was not associated with any major histopathologic subtype of NHL examined, apart from an association between high wine consumption and increased risk of chronic lymphocytic leukemia.Alcohol does not appear to be a major etiologic factor for overall NHL, nor its common subtypes.

    View details for Web of Science ID 000226583100009

    View details for PubMedID 15801490

  • Childhood social environment and Hodgkin's lymphoma: New findings from a population-based case-control study CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Zheng, T. Z., Weir, E. G., Borowitz, M., Mann, R. B., Spiegelman, D., Mueller, N. E. 2004; 13 (8): 1361-1370

    Abstract

    Risk of Hodgkin's lymphoma in young adults has previously been associated with higher childhood socioeconomic status (SES) and other markers of delayed infection with common childhood pathogens, especially the Epstein-Barr virus. This study examines the current role of childhood social environment in the development of Hodgkin's lymphoma.A population-based case-control study of 565 Hodgkin's lymphoma cases and 679 controls was conducted in the Boston, MA metropolitan area and the state of Connecticut to investigate the viral etiology of Hodgkin's lymphoma.A novel association was detected between attendance of nursery school or day care and reduced risk of Hodgkin's lymphoma among individuals ages 15 to 54 years. The odds ratio (95% confidence interval) for having attended preschool for at least 1 year was 0.64 (0.45-0.92). Risk of young-adult Hodgkin's lymphoma was also associated with family history of hematopoietic cancer, Jewish ethnicity, and cigarette smoking. Other indicators of childhood SES were not associated with young-adult Hodgkin's lymphoma. Among older adults ages 55 to 79 years, Hodgkin's lymphoma was associated with lower childhood SES but not with preschool attendance.Early exposure to other children at nursery school and day care seems to decrease the risk of Hodgkin's lymphoma in young adults, most likely by facilitating childhood exposure to common infections and promoting maturation of cellular immunity. This finding supports the delayed infection model of Hodgkin's lymphoma etiology in young adults while introducing a new major determinant of age at infection. Hodgkin's lymphoma seems to have a separate pathogenesis among older adults.

    View details for Web of Science ID 000223155500016

    View details for PubMedID 15298959

  • Re: Zinc supplement use and risk of prostate cancer JOURNAL OF THE NATIONAL CANCER INSTITUTE Chang, E. T., Hedelin, M., Adami, H. O., Gronberg, H., Balter, K. A. 2004; 96 (14): 1108-1108

    View details for DOI 10.1093/jnci/djh206

    View details for Web of Science ID 000222802600016

    View details for PubMedID 15265974

  • Number of siblings and risk of Hodgkin's lymphoma CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION Chang, E. T., Montgomery, S. M., Richiardi, L., Ehlin, A., Ekbom, A., Lambe, M. 2004; 13 (7): 1236-1243

    Abstract

    Epidemiologic evidence indicates that risk of Hodgkin's lymphoma (HL) in young adults is associated with correlates of delayed exposure to infection during childhood. In contrast, HL among children and older adults may be associated with earlier childhood infection. This study examines the associations of HL risk with having older or younger siblings.We conducted a case-control study in Sweden comparing 2,140 HL patients identified from the Swedish Cancer Register with 10,024 controls identified from national population registers. The Swedish Multi-Generation Register was used to link individuals to their parents and siblings.Among young adults ages 15 to 39 years, the odds ratios (OR) associated with having one, two, and three or more older siblings, compared with none, were 0.96 [95% confidence interval (CI), 0.82-1.13], 0.88 (95% CI, 0.72-1.09), and 0.72 (95% CI, 0.55-0.93), respectively (P value for trend = 0.01). In contrast, number of older siblings was not associated with HL risk among children or older adults. Number of younger or total siblings, mother's age at birth, and father's occupation were not associated with HL at any age. The decreased risk of young-adult HL did not vary appreciably by age difference or sex of older siblings.Risk of HL was lower among young adults with multiple older but not younger siblings. Having older siblings is associated with earlier exposure to common childhood pathogens. Pediatric and older-adult HL were not associated with number of siblings, suggesting a different pathogenesis of disease in these age groups.

    View details for Web of Science ID 000222539400020

    View details for PubMedID 15247136

  • Heterogeneity of risk factors and antibody profiles in Epstein-Barr virus genome-positive and -negative Hodgkin lymphoma JOURNAL OF INFECTIOUS DISEASES Chang, E. T., Zheng, T. Z., Lennette, E. T., Weir, E. G., Borowitz, M., Mann, R. B., Spiegelman, D., Mueller, N. E. 2004; 189 (12): 2271-2281

    Abstract

    Hodgkin lymphoma (HL) tumors that contain the Epstein-Barr virus (EBV) genome may differ etiologically from EBV-negative HL tumors.A case-case study examining heterogeneity of risk factors between disease subgroups compared personal characteristics and EBV antibodies between 95 EBV-positive and 303 EBV-negative patients with HL.We confirmed previous associations of EBV-positive HL with older age, male sex, and mixed-cellularity (MC) histological subtypes. EBV-positive patients were less educated and more likely to have smoked cigarettes and had more prevalent and higher EBV antibody titers, compared with EBV-negative patients. After adjustment for all independent risk factors, those most strongly associated with EBV-positive HL were histological subtypes (odds ratio [OR] for MC vs. nodular sclerosis histology, 3.2; 95% confidence interval [CI], 1.4-7.2), elevated anti-viral capsid antigen level (OR, 3.1; 95% CI, 1.6-6.0), and less education (OR, 0.7; 95% CI, 0.5-1.0). Cigarette smoking and a low anti-Epstein-Barr nuclear protein (EBNA) 1 : anti-EBNA-2 ratio were also marginally associated with EBV-positive HL.EBV-positive HL is more common among individuals who have markers of diminished cellular immunity and an abnormal EBV antibody response. EBV appears to participate in the etiology of EBV-positive HL but may not be involved in EBV-negative HL.

    View details for Web of Science ID 000221699500016

    View details for PubMedID 15181575

  • Aspirin and the risk of Hodgkin's lymphoma in a population-based case-control study JOURNAL OF THE NATIONAL CANCER INSTITUTE Chang, E. T., Zheng, T. Z., Weir, E. G., Borowitz, M., Mann, R. B., Spiegelman, D., Mueller, N. E. 2004; 96 (4): 305-315

    Abstract

    Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with decreased risk of several malignancies. NSAIDs may prevent cancer development by blocking the cyclooxygenase-catalyzed synthesis of proinflammatory prostaglandins. Aspirin may also protect against Hodgkin's lymphoma by inhibiting transcription factor nuclear factor kappaB (NF-kappaB), which is necessary for immune function and the survival of Hodgkin's lymphoma cells. We examined the association between regular analgesic use and the risk of Hodgkin's lymphoma.A population-based case-control study of 565 case patients with Hodgkin's lymphoma and 679 control subjects was conducted in the metropolitan area of Boston, Massachusetts, and in the state of Connecticut. Participants reported their average use of aspirin, non-aspirin NSAIDs, and acetaminophen over the previous 5 years. Regular analgesic use was defined as consumption of at least two tablets per week on average over the preceding 5 years; non-regular use was defined as consumption of fewer than two tablets per week.The risk of Hodgkin's lymphoma associated with regular aspirin use was statistically significantly lower (odds ratio [OR] = 0.60, 95% confidence interval [CI] = 0.42 to 0.85) than that associated with non-regular aspirin use. The risk was not associated with use of other non-aspirin NSAIDs (OR = 0.97, 95% CI = 0.73 to 1.30). However, the risk associated with regular acetaminophen use was statistically significantly higher (OR = 1.72, 95% CI = 1.29 to 2.31) than that associated with non-regular use.The inverse association between aspirin, but not other NSAIDs, and Hodgkin's lymphoma suggests that NF-kappaB signaling may play a key role in Hodgkin's lymphoma pathogenesis.

    View details for DOI 10.1093/jnci/djh038

    View details for Web of Science ID 000188953800012

    View details for PubMedID 14970279

  • Immunological quantitation and localization of ACAT-1 and ACAT-2 in human liver and small intestine JOURNAL OF BIOLOGICAL CHEMISTRY Chang, C. C., Sakashita, N., Ornvold, K., Lee, O., Chang, E. T., Dong, R., Lin, S., Lee, C. Y., Strom, S. C., Kashyap, R., Fung, J. J., Farese, R. V., Patoiseau, J. F., Delhon, A., Chang, T. Y. 2000; 275 (36): 28083-28092

    Abstract

    By using specific anti-ACAT-1 antibodies in immunodepletion studies, we previously found that ACAT-1, a 50-kDa protein, plays a major catalytic role in the adult human liver, adrenal glands, macrophages, and kidneys but not in the intestine. Acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity in the intestine may be largely derived from a different ACAT protein. To test this hypothesis, we produced specific polyclonal anti-ACAT-2 antibodies that quantitatively immunodepleted human ACAT-2, a 46-kDa protein expressed in Chinese hamster ovary cells. In hepatocyte-like HepG2 cells, ACAT-1 comprises 85-90% of the total ACAT activity, with the remainder attributed to ACAT-2. In adult intestines, most of the ACAT activity can be immunodepleted by anti-ACAT-2. ACAT-1 and ACAT-2 do not form hetero-oligomeric complexes. In differentiating intestinal enterocyte-like Caco-2 cells, ACAT-2 protein content increases by 5-10-fold in 6 days, whereas ACAT-1 protein content remains relatively constant. In the small intestine, ACAT-2 is concentrated at the apices of the villi, whereas ACAT-1 is uniformly distributed along the villus-crypt axis. In the human liver, ACAT-1 is present in both fetal and adult hepatocytes. In contrast, ACAT-2 is evident in fetal but not adult hepatocytes. Our results collectively suggest that in humans, ACAT-2 performs significant catalytic roles in the fetal liver and in intestinal enterocytes.

    View details for Web of Science ID 000089197100074

    View details for PubMedID 10846185

  • Recombinant acyl-CoA : cholesterol acyltransferase-1 (ACAT-1) purified to essential homogeneity utilizes cholesterol in mixed micelles or in vesicles in a highly cooperative manner JOURNAL OF BIOLOGICAL CHEMISTRY Chang, C. C., Lee, C. Y., Chang, E. T., Cruz, J. C., Levesque, M. C., Chang, T. Y. 1998; 273 (52): 35132-35141

    Abstract

    Acyl-coenzyme A:cholesterol acyltransferase (ACAT) is an integral membrane protein located in the endoplasmic reticulum. It catalyzes the formation of cholesteryl esters from cholesterol and long-chain fatty acyl coenzyme A. The first gene encoding the enzyme, designated as ACAT-1, was identified in 1993 through an expression cloning approach. We isolated a Chinese hamster ovary cell line that stably expresses the recombinant human ACAT-1 protein bearing an N-terminal hexahistidine tag. We purified this enzyme approximately 7000-fold from crude cell extracts by first solubilizing the cell membranes with the zwitterionic detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, then proceeding with an ACAT-1 monoclonal antibody affinity column and an immobilized metal affinity column. The final preparation is enzymologically active and migrates as a single band at 54 kDa on SDS-polyacrylamide gel electrophoresis. Pure ACAT-1 dispersed in mixed micelles containing sodium taurocholate, phosphatidylcholine, and cholesterol remains catalytically active. The cholesterol substrate saturation curves of the enzyme assayed either in mixed micelles or in reconstituted vesicles are both highly sigmoidal. The oleoyl-coenzyme A substrate saturation curves of the enzyme assayed under the same conditions are both hyperbolic. These results support the hypothesis that ACAT is an allosteric enzyme regulated by cholesterol.

    View details for Web of Science ID 000077719700067

    View details for PubMedID 9857049

  • A novel 160-kDa phosphotyrosine protein in insulin-treated embryonic kidney cells is a new member of the insulin receptor substrate family JOURNAL OF BIOLOGICAL CHEMISTRY Lavan, B. E., Fantin, V. R., Chang, E. T., Lane, W. S., Keller, S. R., Lienhard, G. E. 1997; 272 (34): 21403-21407

    Abstract

    We have previously identified a 160-kDa protein in human embryonic kidney (HEK) 293 cells that undergoes rapid tyrosine phosphorylation in response to insulin (PY160) (Kuhné, M. R., Zhao, Z., and Lienhard, G. E. (1995) Biochem. Biophys. Res. Commun. 211, 190-197). The phosphotyrosine form of PY160 was purified from insulin-treated HEK 293 cells by anti-phosphotyrosine immunoaffinity chromatography, the sequences of peptides determined, and its cDNA cloned. The PY160 cDNA encodes a 1257-amino acid protein that contains, in order from its N terminus, a pleckstrin homology (PH) domain, a phosphotyrosine binding (PTB) domain, and, spread over the C-terminal portion, 12 potential tyrosine phosphorylation sites. Several of these sites are in motifs expected to bind specific SH2 domain-containing proteins: YXXM (7 sites), phosphatidylinositol 3-kinase; YVNM (1 site), Grb-2; and YIEV (1 site), either the protein-tyrosine phosphatase SHP-2 or phospholipase Cgamma. Furthermore, the PH and PTB domains are highly homologous (at least 40% identical) to those found in insulin receptor substrates 1, 2, and 3 (IRS-1, IRS-2, and IRS-3). Thus, PY160 is a new member of the IRS family, which we have designated IRS-4.

    View details for Web of Science ID A1997XR78900065

    View details for PubMedID 9261155

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