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Stephanie Markovina
4th year medical student
Cellular & Molecular Biology
8th year of MSTP

smarkovi2@msn.com

EDUCATION

  • B.A. 2001, Washington University
    Biology

RESEARCH EXPERIENCE

  • National Cancer Institute, NIH, 2001-2002
    Advisor - David Gius, PhD, MD
    Project - Continued undergraduate research and more extensively studied components of the pathways.
  • Washington University in St. Louis, 1998 - 2001
    Advisor - David Gius, PhD, MD
    Project - Researched the effects of ionizing radiation, certain chemotherapies, and radio- and chemo- sensitizing agents on tumor cell signalling pathways.

CAREER GOAL

Role of NF-�B in Multiple Myeloma

PUBLICATIONS

  • O'Connor S, Markovina S, Miyamoto S. Evidence for a phosphorylation-independent role for Ser 32 and 36 in proteasome inhibitor-resistant (PIR) IkBa degradation in B cells. Exp Cell Res 307:15-25, 2005.
  • Bisht KS, Bradbury CM, Mattson D, Kaushal A, Sowers A, Markovina S, Ortiz KL, Sieck LK, Isaacs JS, Brechbiel MW, Mitchell JB, Neckers LM, Gius D. Geldanamycin and 17-Allylamino-17-demethoxygeldanamycin potentiate the in vitro and in vivo radiation response of cervical tumor cells via the heat shock protein 90-mediated intracellular signaling and cytotoxicity. Cancer Res 63:8984-95, 2003.
  • Karimpour S, Lou J, Lin LL, Rene LM, Lagunas L, Ma X, Karra S, Bradbury CM, Markovina S, Goswami PC, Spitz DR, Hirota K, Kalvakolanu DV, Yodoi J, Gius D. Thioredoxin reductase regulates AP-1 activity as well as thioredoxin nuclear localization via active cysteines in response to ionizing radiation. Oncogene 21:6317-27, 2002.
  • Bradbury CM, Markovina S, Wei SJ, Rene LM, Zoberi I, Horikoshi N, Gius D. Indomethacin-induced radiosensitization and inhibition of ionizing radiation-induced NF- B activation in HeLa cells occur via a mechanism involving p38 MAP kinase. Cancer Res 61:7689-96, 2001.
  • Wei SJ, Botero A, Hirota K, Bradbury CM, Markovina S, Laszlo A, Spitz DR, Goswami PC, Yodoim J, Gius D. Thioredoxin nuclear translocation and interaction with redox factor-1 activates the activator protein-1 transcription factor in response to ionizing radiation. Cancer Res 60:6688-95, 2000.