I am an Associate Professor of Medicine at Harvard Medical School and co-director of the Cancer Cell Biology Program. My specific expertise is in the Ras pathway, one of the most commonly deregulated signaling pathways in human cancer.
My lab studies this pathway in many tumor types, including sarcomas, glioblastomas, prostate, lung and breast cancers. We have extensively investigated the NF1 tumor suppressor, a Ras-regulatory gene that is mutated in neurofibromatosis, a familial cancer syndrome for which there are few therapies. We have identified a new therapeutic target and demonstrated an effective therapy in mice for the most deadly NF tumor type. These findings inspired several clinical trials and we continue to investigate new therapies and therapeutic combinations for the disorder. We are also investigating the effects of such combinations on other Ras-driven cancers (e.g. lung), and are working with pharmaceutical companies and clinicians to evaluate them in trials. We’ve shown that the mechanism by which NF1 is inactivated affects sensitivity to specific therapeutic agents. We have also been studying NF1-related genes and have identified two new tumor suppressors within this family, and found that one of them underlies metastatic prostate cancer. We’ve discovered that mutations in this gene drive a broad spectrum of tumor-types, and that inactivation of a third gene within this family promotes breast cancer.
I have received several awards for my research, including the Translational Science Award of the Children’s Tumor Foundation and the Innovative Research Idea Prize, National Neurofibromatosis Foundation.
Ludwig Center at Harvard
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