BFAM Member Spotlights

Meet the members of the Stanford Medicine Black Faculty Affinity Meetings (BFAM), a network created through OFDD's Community Support Initiative. BFAM is intended to provide networking and social engagement opportunities for Stanford Medicine faculty across all clinical lines and departments.

Marvin Langston, PhD, MPH

Epidemiology and Population Health

Assistant Professor of Epidemiology and Population Health

Research Interests
Epidemiology of Prostate Cancer and Benign Prostate Conditions; Health Equity; Causal Inference Approaches

Something you wouldn’t know just by looking at me
I’m a huge politico. I have probably read the memoirs of most major politicians over the last 10 years or so from both ends of the political spectrum.

What are some of your favorite restaurants?
San Tung, Horn BBQ, Minnie Bells Soul Movement

What are some of your favorite social activities?
Warriors games, bar hopping around Oakland, and playing tennis with friends

Full Stanford Profile

Assistant Professor of Epidemiology and Population Health

marvlang@stanford.edu

Bio

Dr. Marvin Langston is an Assistant Professor of Epidemiology and Population Health. He is a member of the Stanford Cancer Institute and Urologic Cancer Epidemiology Lab. He is an epidemiologist by training who focuses on the fields of benign prostate and pelvic conditions and urological cancers including prostate and kidney cancers. Prior to Stanford, he served as a Research Scientist in the Division of Research at Kaiser Permanente Northern California. Dr. Langston received his PhD in Epidemiology from the University of Arizona’s College of Public Health followed by postdoctoral training in Cancer Prevention and Control at Washington University in Saint Louis School of Medicine. His program of research intends to characterize and measure infectious agents, environmental toxicants, and lifestyle factors; to evaluate the role of these factors in urological cancer etiology and outcomes; and to identify populations at high risk of exposure to these factors. So far he has focused this research to address the following questions: 1) What role do sexually transmitted infections and other systemic infections have in prostate damage and ensuing prostate cancer risk? 2) How can we appropriately model and define early life risk factors for urological cancers? 3) Can we harmonize molecular and clinical aspects of urological condition diagnoses to produce well characterized outcomes for biomarker discovery and etiological investigation? He has primarily addressed these questions using a variety of molecular and clinical epidemiology approaches while developing expertise in the cross-cutting theme of cancer health disparities with particular interests in the cancer care experiences of sexual and gender minorities and racial/ethnic minorities. Dr. Langston has been studying the impact of exogenous factors on prostate specific antigen (PSA) concentration in young men as a marker of prostate damage and inflammation for over a decade. As early life PSA has been found predictive of future prostate cancer mortality, he has now setout to optimize risk-stratified screening for prostate cancer. This promising approach uses men’s baseline PSA values to inform their risk of future aggressive and/or fatal prostate cancer and determine their frequency of further screening. Under this approach, men with high baseline age-specific total PSA levels receive more frequent screening and men with lower levels receive less frequent screening. Dr. Langston was awarded an R01 from NCI to evaluate this approach using historically collected biospecimen. His funded research trajectory to this point also includes four training awards (2-NCI and 2-NIDDK) and several internal grants. Dr. Langston was selected in the inaugural class of the White House Cancer Moonshot Scholars for his work.

Publications

Polygenic score for body mass index in relation to mortality among patients with renal cell cancer. International journal of obesity (2005) Deng, Z., Graff, R. E., Batai, K., Chung, B. I., Langston, M. E., Kachuri, L. 2024 More

Abstract

The association between body mass index (BMI) and mortality among individuals with renal cell cancer (RCC) is debated, with some observational studies suggesting a lower mortality associated with higher BMI. However, methodological issues such as confounding and reverse causation may bias these findings. Using BMI-associated genetic variants can avoid these biases and generate more valid estimates.In this prospective cohort study, we included 1264 RCC patients (446 deaths) from the UK Biobank. We created a BMI polygenic score (PGS) based on 336 BMI-associated genetic variants. The association between the PGS and mortality (all-cause and RCC-specific) was evaluated by logistic regression (all RCC cases) and Cox regression (906 incident cases). For comparison, the associations of measured pre-diagnostic BMI and waist-to-hip ratio (WHR) with mortality were quantified by Cox regression among incident cases. We stratified these analyses by time between anthropometric measurement and RCC diagnosis to assess the influence of reverse causation.We did not observe an association between the BMI PGS and all-cause mortality among RCC patients (hazard ratio (HR) per SD increase = 0.98, 95% CI: 0.88,1.10). No association was found for pre-diagnostic BMI (HR per 5 kg/m2 increase = 0.93, 95% CI: 0.83,1.04) or WHR (HR per 0.1 increase = 0.97, 95% CI: 0.83,1.13) with mortality. In patients with anthropometrics measured within 2 years before RCC diagnosis, we observed associations of higher BMI (HR per 5 kg/m2 = 0.76, 95% CI: 0.59,0.98) and WHR (HR = 0.67 per 0.1 increase, 95% CI: 0.45,0.98) with a lower risk of death. Similar patterns were observed for RCC-specific mortality.We found no association between either genetic variants for high BMI or measured pre-diagnostic body adiposity and mortality among RCC patients, and our results suggested a role for reverse causation in the association of obesity with lower mortality. Future studies should be designed carefully to produce unbiased estimates that account for confounding and reverse causation.

View details for DOI 10.1038/s41366-024-01609-0

View details for PubMedID 39152336

View details for PubMedCentralID 6221676
Increased risk of cardiovascular disease among kidney cancer survivors: a nationwide population-based cohort study. Frontiers in oncology Jung, M., Choo, E., Li, S., Deng, Z., Li, J., Li, M., Basran, S., Lee, S., Langston, M. E., Chung, B. I. 2024; 14: 1420333 More

Abstract

Cardiovascular disease (CVD) is a major concern of morbidity and mortality among cancer survivors. However, few evidence exists on the short- and long-term risk of CVD in kidney cancer (KCa) survivors.In this nationwide, large population-based retrospective cohort study, we used the Korean national health insurance and medical checkup survey linkage database (2007-2021), drawn from the entire Korean population. We included adults diagnosed with KCa as the first primary cancer and matched them to an individual without KCa at a 1:5 ratio. The primary outcome was CVD incidence, including myocardial infarction, stroke, atrial fibrillation, heart failure, peripheral arterial occlusion, and venous thromboembolism (VTE). We evaluated CVD risk at 6 months, 1 year, and 5 years following cancer diagnosis, using Fine-Gray competing risk models that accounted for death as a competing factor.A total of 149,232 participants were included (KCa survivors: N=20,093 and matched non-KCa individuals: N=129,139). After 6-month follow-up, KCa survivors showed an increased risk of CVD compared to the general population (subdistribution hazard ratio (HR) 2.70, 95% confidence interval (CI) 2.31-3.15). After 1 year, KCa survivors had a higher risk of CVD (HR=1.77, 95% CI: 1.56-2.00). After 5 years, this elevated CVD risk remained (HR=1.10, 95% CI: 1.03-1.18), with VTE identified as the primary contributing disease (HR=3.05, 95% CI:2.59-3.59).KCa survivors had an increased risk of CVD up to 5 years after cancer diagnosis compared to the general population. Our findings emphasize the importance of comprehensive healthcare management for both CVD and KCa throughout cancer survivorship.

View details for DOI 10.3389/fonc.2024.1420333

View details for PubMedID 39070148

View details for PubMedCentralID PMC11272517
Ambient air pollution and urological cancer risk: A systematic review and meta-analysis of epidemiological evidence. Nature communications Li, J., Deng, Z., Soerensen, S. J., Kachuri, L., Cardenas, A., Graff, R. E., Leppert, J. T., Langston, M. E., Chung, B. I. 2024; 15 (1): 5116 More

Abstract

Exposure to ambient air pollution has significant adverse health effects; however, whether air pollution is associated with urological cancer is largely unknown. We conduct a systematic review and meta-analysis with epidemiological studies, showing that a 5 μg/m3 increase in PM2.5 exposure is associated with a 6%, 7%, and 9%, increased risk of overall urological, bladder, and kidney cancer, respectively; and a 10 μg/m3 increase in NO2 is linked to a 3%, 4%, and 4% higher risk of overall urological, bladder, and prostate cancer, respectively. Were these associations to reflect causal relationships, lowering PM2.5 levels to 5.8 μg/m3 could reduce the age-standardized rate of urological cancer by 1.5 ~ 27/100,000 across the 15 countries with the highest PM2.5 level from the top 30 countries with the highest urological cancer burden. Implementing global health policies that can improve air quality could potentially reduce the risk of urologic cancer and alleviate its burden.

View details for DOI 10.1038/s41467-024-48857-2

View details for PubMedID 38879581

View details for PubMedCentralID PMC11180144
Response to Letter to the Editor. The journals of gerontology. Series A, Biological sciences and medical sciences Bauer, S. R., Langston, M. E., Ferrucci, L., Simonsick, E. M. 2024; 79 (6) More

View details for DOI 10.1093/gerona/glae103

View details for PubMedID 38758044
Air pollution mixture associated with oxidative stress exacerbation and symptoms deterioration in allergic rhinitis patients: Evidence from a panel study. The Science of the total environment Li, J., Wu, H., Xing, W., Li, X., Han, Z., Ji, R., Deng, Z., Jung, M., Sun, S., Chung, B. I., Cardenas, A., Langston, M. E. 2024: 172688 More

Abstract

With allergic rhinitis (AR) on the rise globally, there has been a growing focus on the role of environmental pollutants in the onset of AR. However, the potential mechanisms by how and which these pollutants exacerbate AR conditions remain unknown. This panel study of 49 patients diagnosed with AR over one year aimed to assess the individual and combined effects of short-term exposure to multiple ambient pollutants on oxidative stress, symptoms, and quality of life among patients with AR. All participants underwent four repeated assessments of health conditions and personal environmental exposures (PM2.5, O3, SO2, and NO2) over warm and cold seasons during 2017-2018. We evaluated two oxidative stress biomarkers (malondialdehyde [MDA], and superoxide dismutase [SOD]) via nasal lavage. We collected information on self-reported symptoms and quality of life using the Rhinitis Symptom Scale (SRS), the Visual Analog Scale (VAS), and the Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) through in-person interviews. Bayesian kernel machine regression (BKMR) was used to evaluate the joint effects of pollutant mixture and identify key contributors. The results revealed a significant association of the pollutant mixture when all four pollutants were at or above their median levels, with increased oxidative stress. This was evidenced by elevated MDA and reduced SOD. We found a joint detrimental effect of the pollutant mixture on AR symptoms with a strong association with increased SRS scores, but a non-significant positive association with VAS and RQLQ scores. PM2.5, O3, and SO2 presented as the potentially primary contributors to the adverse health effects associated with the pollutant mixture in Taiyuan city. Patients with AR exposed to short-term air pollutant mixture are more likely to have greater nasal symptoms and worse quality of life from increased oxidative stress and reduced antioxidant capacity. Further research is warranted to better elucidate the underlying mechanisms.

View details for DOI 10.1016/j.scitotenv.2024.172688

View details for PubMedID 38663627

see all 43 publications

BFAM Member Spotlights

Marvin Langston, PhD, MPH

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