Brian J. Druker, M.D.
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- Phone:
- 503 494-7999
- Office:
- 503 494-5058
Background
Dr. Druker's research focuses on activated tyrosine kinases with an emphasis on signal transduction and cellular transformation and the application of this knowledge to cancer therapies. The BCR-ABL oncogene is his lab's primary model system because of its central role in the pathogenesis of a human disease, chronic myeloid leukemia (CML). Numerous tyrosine phosphorylated proteins have been identified in BCR-ABL transformed cells and projects are ongoing to define their necessity for BCR-ABL function. These studies include mutational, biochemical and genetic approaches. Imatinib (Gleevec), a specific inhibitor of the ABL protein tyrosine kinase, has been proven to be an effective therapeutic agent in CML. However, it is not capable of eliminating all leukemic cells. In laboratory correlate studies done alongside imatinib clinical trials, Dr. Druker's lab learned that ABL kinase domain mutations are the most common mechanism of resistance to imatinib. Using this information, his team has evaluated several novel ABL inhibitors that are now available to treat patients with Gleevec resistance. Lastly, Dr. Druker's lab is performing screens for other tyrosine kinases that may be pathogenic in other leukemias and has developed functional assays that allow rapid target identification.
Summary of Current Research
Special Interests Chronic myeloid leukemia
Selected Publications
"Imatinib and dasatinib inhibit hemangiosarcoma and implicate PDGFR-β and Src in tumor growth,"
"HitWalker: Variant prioritization for personalized functional cancer genomics,"
"The selective syk inhibitor P505-15 (PRT062607) inhibits B cell signaling and function in vitro and in vivo and augments the activity of fludarabine in chronic lymphocytic leukemias,"
"BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: Frequency and clonal relationships,"
"Kinase pathway dependence in primary human leukemias determined by rapid inhibitor screening,"
