Vivian G. Oehler
Fellowship Training, University of Washington, Hematology and Oncology, 2004.
Fellowship Training, Fred Hutchinson Cancer Research Center, Hematology and Oncology, 2004.
Residency Training, University of Washington, Medicine, 2000.
M.D., Case Western Reserve University, Medicine, 1997.
B.A., Harvard University, Government, 1989.
Current Clinical Interests
Myeloproliferative and myelodysplastic disorders; acute myeloid leukemia
Current Research Interests
Mechanisms of leukemia disease initiation/progression and therapy resistance, new agents in the treatment of chronic myeloid leukemia (CML) and acute myeloid leukemia (AML).
Tyrosine kinase inhibitors such as imatinib, dasatinib and nilotinib 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 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 have identified similar changes in AML. 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. To answer the second question, the most promising candidates derived from our patient-based studies are examined in vitro and in vivo to better understand their possible function in disease progression and therapy resistance, and to define pathways that can be targeted by existing or novel therapies.
Reading, Writing, Speaking
German: Fluent, Functional, Fluent
American Society of Hematology
Southwest Oncology Group
Honors and Awards
Honor Medical Society, Alpha Omega Alpha
Clinical/Translational Research Scholar Award, American Society of Hematology - Fellow Award
2008-2008, Acting Assistant Professor, University of Washington, School of Medicine, Medicine, Hematology
2005-2008, Associate in Clinical Research, Fred Hutchinson Cancer Research Center, Clinical Research Division
2004-2005, Research Associate, Fred Hutchinson Cancer Research Center
2004-2008, Acting Instructor, University of Washington, School of Medicine, Medicine, Hematology
Prognostic significance of NPM1 mutations in the absence of FLT3-internal tandem duplication in older patients with acute myeloid leukemia: a SWOG and UK National Cancer Research Institute/Medical Research Council report.. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 33(10):1157-64.. 2015.
The prognostic significance of IRF8 transcripts in adult patients with acute myeloid leukemia.. PloS one. 8(8):e70812.. 2013.
Update on current monitoring recommendations in chronic myeloid leukemia: practical points for clinical practice.. Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program. 2013:176-83.. 2013.
Higher dose imatinib for children with de novo chronic phase chronic myelogenous leukemia: a report from the Children's Oncology Group.. Pediatric blood & cancer. 57(1):56-62.. 2011.
Molecular alterations of the IDH1 gene in AML: a Children's Oncology Group and Southwest Oncology Group study.. Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 24(5):909-13.. 2010.
Regulation of myeloid leukaemia by the cell-fate determinant Musashi.. Nature. 466(7307):765-8.. 2010.