Research Interests

For over two decades, my colleagues and I have used molecular genetics to clarify the molecular basis of cancer, focussing on the role of chromosome translocations in lymphoma development. We (and others) discovered that the hallmark translocation in Burkitt lymphoma activates the Myc proto-oncogene by coupling it to an immunoglobulin locus. To prove its etiological role, we showed that mice bearing a Myc transgene that mimics the chromosome junction are highly predisposed to lymphomagenesis. These transgenic mice and others we developed have proven very effective for dissecting tumorigenesis and, more recently, for studying new approaches to therapy. Our most influential discovery has been the critical role of impaired cell death in cancer development and resistance to therapy. Our laboratory revealed that the Bcl-2 gene, discovered by others via its translocation in follicular lymphoma, was oncogenic because it imposes cell survival. Bcl-2 has proven to be the prototype of a family of proteins whose interactions arbitrate the life and death of cells. We are now attempting to clarify how those interactions flip the cell death (apoptosis) switch, how the effectiveness of that switch is impaired in cancer cells and how it can be reactivated to improve cancer treatment.

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Section 41: Medical Genetics, Hematology, and Oncology