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Education and Training:

B.A. in Government, Harvard University (1985-89)

Post-baccalaureate premed courses, S.U.N.Y. (1990-92)

M.D., Case Western Reserve University School of Medicine (1993-97)

Internship, Internal Medicine, University of Washington Affiliated Hospital, Seattle, WA (1997-98)

Residency, Internal Medicine University of Washington Affiliated Hospitals (1998-00)

Hematology Fellowship, University of Washington Affiliated Hospitals (2000-04)

Post-Doctoral Research Fellow, Jerald Radich Laboratory, FHCRC (2002-04)

 

Vivian G. Oehler, M.D.
Assistant Member
Fred Hutchinson Cancer Research Center

Assistant Professor of Medicine
Division of Hematology
University of Washington School of Medicine

Office Address:
Fred Hutchinson Cancer Research Center
1100 Fairview Ave., N., D5-100
Seattle, WA 98109

Phone:  (206) 667-1340
Fax:      (206) 667-2917
E-mail:  voehler@u.washington.edu


CURRENT CLINICAL INTERESTS

Myeloproliferative and myelodysplastic disorders; acute myeloid leukemia


CURRENT RESEARCH INTERESTS

Mechanisms of leukemic disease progression and therapy resistance, new agents in the treatment of chronic myeloid leukemia (CML) and acute myeloid leukemia (AML)


RESEARCH DESCRIPTION

The tyrosine kinase inhibitor imatinib mesylate (Gleevec), and now the second generation tyrosine kinase inhibitors 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 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.  Expression of these diagnostic markers is correlated with other clinical and molecular markers such bcr-abl mRNA response and the development of ABL tyrosine kinase domain point mutations (a common mechanism of resistance).  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.  We believe the findings and methodologies utilized here can be extended to the study, monitoring, and treatment of other cancers


SELECTED PUBLICATIONS

Oehler VG*, Yeung KY*, Choi E, Bumgarner RE, Raftery AE, et al.  The derivation of diagnostic markers of chronic myeloid leukemia progression from microarray data.  Blood.  2009; prepublished online August 4, 2009.  PMID 9654405.   * These authors had equal participation in the work.

Oehler VG, Guthrie K, Cummings CL, Sabo K, Wood BL, et al.  Preferentially Expressed Antigen in Melanoma (PRAME) inhibits myeloid differentiation in normal hematopoietic and leukemic progenitor cells.  Blood. 2009; prepublished online July 22, 2009. PMID 19625708.

Oehler VG, Qin J, Ramakrishnan R, Facer G, Ananthnarayan S, et al.  Absolute quantitative detection of ABL tyrosine kinase domain point mutations using a novel nanofluidic platform and mutation-specific PCR.  Leukemia. 2009; 23:396-399.  PMID 18615105.

Oehler V and Radich JP.  Monitoring chronic myeloid leukemia in the age of tyrosine kinase inhibitors.  JNCCN.  2007; 5:497-504. PMID 17509253

Oehler V, Radich JP.  Monitoring of patients with chronic myeloid leukemia receiving Abl tyrosine kinase inhibitor therapy.  Clin Lymphoma Myeloma.  2007; Suppl 2: S58-63.  PMID 17382014.

Oehler VG, Gooley T, Snyder DS, Johnston L, Lin A, Cummings CC, et al.  The effects of imatinib mesylate treatment before allogeneic transplantation for chronic myeloid leukemia.  Blood. 2007; 109:1782-1789.  PMID 17062727.

Radich JP, Dai H, Mao M, Oehler V, Schelter J, et al.  Gene expression changes associated with progression and response in chronic myeloid leukemia.  Proc Natl Acad Sci USA.  2006; 103:2794-2799.  PMID 16477019.