Osteoclasts are central to the pathogenesis of skeletal metastases. Pharmacologic blockade of osteoclast function and development using bisphosphonates can result in decreases in bone metastases, fractures and bone pain. My laboratory studies the transcriptional regulation of osteoclast development to identify novel targets for therapeutic intervention in bone metastases from breast and prostate cancer. The Microphthalmia transcription factor (Mitf) and the related protein TFE3 are critical to osteoclast fusion and maturation. We study the signaling of Macrophage colony stimulating factor (M-CSF) and RANKL, two vital osteoclastogenic factors, with the Microphthalmia transcription factor family and its nuclear target genes. We are also developing animal models of bone metastases using osteopetrotic mouse mutants and other genetically targeted osteoclast mutants. Key words: Breast cancer, bone metastases, osteoclast development, beta 3 integrin signaling, microphthalmia transcription factor, RANKL signaling, osteolytic and osteoblastic bone metastases, bone marrow metastases.
- 1992: MD, Stanford University, Stanford, Calif.
- 1992 - 1994: Intern and resident, internal medicine, Stanford University Hospital, Stanford, Calif.
- 1994 - 1998: Fellow, medical oncology, Dana-Farber Cancer Institute, Boston
- 1994 - 1998: Clinical fellow, internal medicine, Brigham and Women's Hospital and Harvard Medical School, Boston
- 1995: American Board of Internal Medicine, Internal Medicine
- 1997: American Board of Internal Medicine, Medical Oncology