Bio

Clinical Focus


  • General Internal Medicine
  • Internal Medicine

Academic Appointments


Administrative Appointments


  • Clinical Assistant Professor, Stanford Medical School (2009 - Present)
  • Clinical Instructor, Stanford Medical School (2006 - 2009)
  • Clinical Instructor, Stanford Medical School (2005 - 2005)
  • Medical Staff, Palo Alto Veteran Affairs Hospital (2004 - 2008)

Honors & Awards


  • DGIM research award, Stanford Department of General Internal Medicine (2010)
  • Exceptional Preceptor in the Ambulatory Medicine Clerkship, Stanford University (2006)
  • Erasmus scholarship to study medicine in a foreign country, ERASMUS Programme (1997)

Professional Education


  • Residency:Stanford University Medical Center (2004) CA
  • Board Certification: Internal Medicine, American Board of Internal Medicine (2004)
  • Internship:Stanford University Medical Center (2002) CA
  • Residency:Medizinische Hochschule Hannover (1999) Germany
  • Medical Education:Georg-August University Faculty Medicine (1997) Germany
  • Residency, Stanford Medical School, Internship and Residency (2004)
  • Fellow, Stanford University, Postdoctoral Fellow (2001)
  • Fellow, Dana-Farber Cancer Institute, Postdoctoral Fellow (2000)
  • Postgrad, Medical University of Hannover, Internal Medicine (1999)
  • M.D., Georg August University, Doctoral Thesis (1997)
  • M.D., Georg August University, Medical School (1997)

Community and International Work


  • Teaching Module, Stanford University

    Topic

    Abnormal Vaginal Bleeding

    Populations Served

    Internal Publication

    Location

    California

    Ongoing Project

    No

    Opportunities for Student Involvement

    No

  • Teaching Module, Stanford University

    Topic

    The Abnormal Pap Smear in the Internist's Office

    Populations Served

    Internal Publication

    Location

    California

    Ongoing Project

    No

    Opportunities for Student Involvement

    No

Teaching

2013-14 Courses


Publications

Journal Articles


  • TERT promotes epidermal proliferation through transcriptional control of a Myc- and Wnt-related developmental program. PLoS Genet Choi, J., Southworth, Sarin, K., Venteicher, A.S., Ma, W., Chang, W., Cheung, P., Jun, S., Artandi, M.K., Shah, N., Kim, S 2008: (4) 1
  • Conditional telomerase induction causes proliferation of hair follicle stem cells NATURE Sarin, K. Y., Cheung, P., Gilison, D., Lee, E., Tennen, R. I., Wang, E., Artandi, M. K., Oro, A. E., Artandi, S. E. 2005; 436 (7053): 1048-1052

    Abstract

    TERT, the protein component of telomerase, serves to maintain telomere function through the de novo addition of telomere repeats to chromosome ends, and is reactivated in 90% of human cancers. In normal tissues, TERT is expressed in stem cells and in progenitor cells, but its role in these compartments is not fully understood. Here we show that conditional transgenic induction of TERT in mouse skin epithelium causes a rapid transition from telogen (the resting phase of the hair follicle cycle) to anagen (the active phase), thereby facilitating robust hair growth. TERT overexpression promotes this developmental transition by causing proliferation of quiescent, multipotent stem cells in the hair follicle bulge region. This new function for TERT does not require the telomerase RNA component, which encodes the template for telomere addition, and therefore operates through a mechanism independent of its activity in synthesizing telomere repeats. These data indicate that, in addition to its established role in extending telomeres, TERT can promote proliferation of resting stem cells through a non-canonical pathway.

    View details for DOI 10.1038/nature03836

    View details for Web of Science ID 000231263900057

    View details for PubMedID 16107853

  • Irinotecan combined or alternated with bolus 5-fluorouracil and folinic acid versus the Mayo clinic regimen in the first line therapy of advance colorectal cancer Oncol Rep Graeven U.,, Ridwelski K., Artandi M., Espana P., Scholmerich J et al 2005: 13 (4) 681-8
  • Constitutive telomerase expression promotes mammary carcinomas in aging mice PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Artandi, S. E., Alson, S., Tietze, M. K., Sharpless, N. E., Ye, S., Greenberg, R. A., Castrillon, D. H., Horner, J. W., Weiler, S. R., Carrasco, R. D., DePinho, R. A. 2002; 99 (12): 8191-8196

    Abstract

    Telomerase is up-regulated in the vast majority of human cancers and serves to halt the progressive telomere shortening that ultimately blocks would-be cancer cells from achieving a full malignant phenotype. In contrast to humans, the laboratory mouse possesses long telomeres and, even in early generation telomerase-deficient mice, the level of telomere reserve is sufficient to avert telomere-based checkpoint responses and to permit full malignant progression. These features in the mouse provide an opportunity to determine whether enforced high-level telomerase activity can serve functions that extend beyond its ability to sustain telomere length and function. Here, we report the generation and characterization of transgenic mice that express the catalytic subunit of telomerase (mTERT) at high levels in a broad variety of tissues. Expression of mTERT conferred increased telomerase enzymatic activity in several tissues, including mammary gland, splenocytes, and cultured mouse embryonic fibroblasts. In mouse embryonic fibroblasts, mTERT overexpression extended telomere lengths but did not prevent culture-induced replicative arrest, thus reinforcing the view that this phenomenon is not related to occult telomere shortening. Robust telomerase activity, however, was associated with the spontaneous development of mammary intraepithelial neoplasia and invasive mammary carcinomas in a significant proportion of aged females. These data indicate that enforced mTERT expression can promote the development of spontaneous cancers even in the setting of ample telomere reserve.

    View details for DOI 10.1073/pnas.112515399

    View details for Web of Science ID 000176217700071

    View details for PubMedID 12034875

  • Phase II study of systemic gemcitabine chemotherapy for advanced unresectable hepatobiliary carcinomas HEPATO-GASTROENTEROLOGY Kubicka, S., Rudolph, K. L., Tietze, M. K., Lorenz, M., Manns, M. 2001; 48 (39): 783-789

    Abstract

    Patients with advanced unresectable hepatobiliary carcinomas have a dismal prognosis. The efficacy of systemic chemotherapy in these patients is negligible and often, in particular in patients with hepatocellular carcinomas, the toxicity of chemotherapy outweighs the potential palliative effect of antineoplastic agents. Gemcitabine is a new anticancer agent with a mild toxicity profile, which has demonstrated antineoplastic activity in many solid tumors. Therefore we investigated the effect of gemcitabine in patients with advanced nonresectable hepatocellular and cholangiocellular carcinomas in a phase II study.Twenty-three patients with cholangiocellular carcinoma and 20 patients with hepatocellular carcinoma were enrolled into the study. Eighteen of the 20 patients with hepatocellular carcinomas had liver cirrhosis. Gemcitabine was administered once weekly over 30 min for 3 consecutive weeks out of every 4 weeks. Patients with cholangiocellular carcinomas received gemcitabine also in the forth week of the first cycle with no rest to the following cycle. Disease status was assessed every 4 weeks.Overall the regimen was well tolerated. The median number of gemcitabine administration was 15 (range, 3-37) in the group of patients with cholangiocellular carcinomas and 7.6 (range, 3-21) in the group of patients with hepatocellular carcinomas. In the group of patients with hepatocellular carcinomas thrombocytopenia was the most frequent side effect (30% grade 3/4). Among the patients with cholangiocellular carcinomas nausea and neutropenia were the most commonly observed side effects. The overall response rate of hepatocellular carcinomas was only 5% and chemotherapy generally did not improve the tumor symptoms of the patients in this group. In contrast, in the group of cholangiocellular carcinomas, seven patients achieved a partial response (overall response rate 30%). Eleven patients with cholangiocellular carcinomas revealed tumor symptoms before the onset of gemcitabine treatment. Seven of these patients developed a treatment related clinical benefit as defined as a relief of tumor symptoms or gain of weight.Our results indicate that the treatment of cholangiocarcinomas with gemcitabine is effective and should be further evaluated in phase III studies. In contrast, palliative chemotherapy with gemcitabine cannot be recommended in patients with hepatocellular carcinoma and liver cirrhosis.

    View details for Web of Science ID 000169631600042

    View details for PubMedID 11462924

  • Murine models of malignant melanoma MOLECULAR MEDICINE TODAY Tietze, M. K., Chin, L. 2000; 6 (10): 408-410

    View details for Web of Science ID 000089768000010

    View details for PubMedID 11006531

  • I kappa B alpha gene therapy in tumor necrosis factor-alpha- and chemotherapy-mediated apoptosis of hepatocellular carcinomas CANCER GENE THERAPY Tietze, M. K., Wuestefeld, T., Paul, Y., Zender, L., Trautwein, C., Manns, M. P., Kubicka, S. 2000; 7 (10): 1315-1323

    Abstract

    The transcription factor nuclear factor kappaB (NFkappaB) is an essential antagonist of apoptosis during liver regeneration and embryonal development of hepatocytes. Several reports have indicated that NFkappaB may also inhibit the programmed cell death induced by cytokines, ionizing radiation, or cytotoxic drugs in some cancer cell lines. Because hepatocellular carcinomas (HCCs) are one of the most resistant tumors to systemic chemotherapy, we investigated the activation of NFkappaB and the consequence of its inhibition by an IkappaBalpha-super repressor during tumor necrosis factor alpha (TNFalpha)- and chemotherapy-induced apoptosis in HCC cell lines. We demonstrate that both TNFalpha and adriamycin activate NFkappaB in hepatoma cells. Activation of NFkappaB could be blocked through an adenoviral vector expressing the IkappaBalpha super repressor, regardless of the activating agent. Inhibition of NFkappaB enhanced the apoptosis induced by TNFalpha, whereas IkappaBalpha had an anti-apoptotic effect on chemotherapy-induced programmed cell death. A strong inhibition of chemotherapy- and TNFalpha-induced apoptosis by dominant-negative Fas-associated death domain indicated an essential contribution of death receptor-mediated apoptosis. To elucidate the different role of NFkappaB in chemotherapy-induced apoptosis, we investigated the expression of Fas (CD95) and Fas ligand (CD95 ligand), which have been described as important mediators of chemotherapy-induced cell death and as target genes of NFkappaB. However, our investigations demonstrated that in hepatoma cells, the chemotherapy-induced up-regulation of Fas (CD95) and Fas ligand (CD95 ligand) is not transcriptionally mediated through NFkappaB. Thus, other molecular mechanisms must account for the anti-apoptotic effect of IkappaBalpha in adriamycin-induced death of hepatoma cells. In summary, our investigations indicate that the activation of NFkappaB in response to cytotoxic drugs, in contrast to TNFalpha, exerts a pro-apoptotic stimulus rather than an anti-apoptotic function, which has implications for therapy of HCCs.

    View details for Web of Science ID 000090073200004

    View details for PubMedID 11059688

  • Hepatocellular carcinoma in Germany: a retrospective epidemiological study from a low-endemic area Liver Kubicka S.,, Rudolph KL., Hanke T., Tietzke MK., Tillmann H.., Trautwein C., Manns M. 2000: 20 (4):312-8
  • NfkB mediates apoptosis through transcriptional activation of Fas (CD95) in adenoviral hepatitis J Biol Chem Kuehnel F.,, Zender L., Paul Y., Tietzke MK., Trautwein C., Manns M., Kubicka S. 2000: 275:6421-7

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