This is unpublished

Vivian
Oehler
M.D.

she, her, hers
Physician & Research Faculty
Pinned
Academic
Associate Professor, Division of Hematology and Oncology, University of Washington
Associate Professor, Translational Science and Therapeutics Division, Fred Hutchinson Cancer Center
Sites of Practice
Fred Hutchinson Cancer Center - South Lake Union

Photo: Fred Hutch

education, training, board certifications

  • M.D., Case Western Reserve University
  • Residency in Internal Medicine, University of Washington
  • Fellowship in Hematology, UW
  • Oncology, American Board of Internal Medicine

Clinical expertise

  • Myeloproliferative disorders
  • Myelodysplastic syndrome
  • Acute myeloid leukemia
  • Chronic myeloid leukemia
  • Essential thrombocytosis
  • Aplastic anemia

Affiliations

publications

Clinical and/or research interests

Dr. Vivian Oehler's research delves into the tyrosine kinase inhibitor imatinib mesylate (Gleevec), and now the second generation tyrosine kinase inhibitors dasatinib and nilotinib, which have dramatically altered treatment strategies in chronic myeloid leukemia (CML). Outcomes for early (or chronic phase) disease are excellent. However, a significant minority of chronic phase CML patients and many advanced CML patients develop resistance to therapy. In the laboratory we are examining mechanisms involved in CML disease progression and the effects of tyrosine kinase inhibitor therapy on the underlying natural history of CML disease. In the clinic we are pursuing phase one studies of new agents in the treatment of CML and AML.

CML provides a unique disease model in which to apply a translational approach. Using microarray-based gene and microRNA expression studies of a large group of CML patients, we have identified expression changes in patients that are highly associated with disease progression and therapy resistance. We are using these data to investigate several questions including: can we identify candidates that predict which patients are at risk for early therapy failure or disease progression and can we determine how these genes and their targets cause disease progression and therapy resistance? To answer the first question we are investigating a group of prognostic markers at diagnosis that can identify patients at risk for early disease progression or therapy failure.