Biography
Brian J. Druker, M.D., is the Director of the OHSU Cancer Institute Leukemia Center. As a Professor of Medicine, Division of Hematology and Medical Oncology, he has joint appointments in the Department of Cell and Developmental Biology and the Department of Biochemistry and Molecular Biology. Upon graduating from UC San Diego medical school in 1981, Dr. Druker completed his internship and residency in internal medicine at Barnes Hospital: Washington School of Medicine in St. Louis, Missouri. He then trained in Oncology at Harvard's Dana-Farber Cancer Institute. Upon completion of his clinical training, Dr. Druker returned to the lab to begin a research career studying the regulation of the growth of cancer cells and how this knowledge could be applied to cancer therapies. His work has been instrumental in the development of a drug that has shown remarkable success in the treatment of patients with chronic myeloid leukemia. The clinical trials with STI571, commonly known as Gleevec, have been heralded as a new paradigm in cancer therapy. His role in the development of STI571 and application in the clinic have resulted in numerous awards for Dr. Druker, including the AACR Richard and Hinda Rosenthal Award, the John J. Kenney Award from the Leukemia and Lymphoma Society, the Warren Alpert Prize from Harvard Medical School, and The American Society of Hematology’s Dameshek Prize.
Abstract
Molecularly Targeted Therapies for Leukemia
Molecular studies have identified a number of distinct signal transduction pathways that are deregulated in human cancers. A major priority for the cancer research community is the translation of this growing body of knowledge into therapeutics targeted specifically to these pathways. Our work with STI571, an inhibitor of the molecular pathogenetic tyrosine kinases in chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST) have validated this approach. In performing these clinical trials, we have gained a significant amount of experience in the design and implementation of studies with molecularly targeted agents. These studies have confirmed our opinion that an essential part of these studies are molecular endpoints for determination of optimal therapeutic benefit and that a new paradigm needs to be established in which basic science investigations are an integral part of clinical trials of these agents. Having established this paradigm with STI571, we now are turning our attention to the FLT3 tyrosine kinase, which is constitutively activated by mutation in over 30% of cases of acute myeloid leukemia (AML), making this the most common mutation in AML. Our goals are to identify a suitable FLT3 inhibitor for clinical trials, to prepare all of the reagents necessary for mutation detection and determination of the activation state of FLT3, and perform clinical trials with a FLT3 inhibitor. We believe that our experience with STI571 makes our group uniquely suited to this task.