William G. Kaelin, Jr., MD

2008-2009 BCRF Project:
Proteins that accelerate ("catalyze") specific chemical reactions are called enzymes. Many successful drugs work by inhibiting a specific enzyme (the drug's "target"). Indirect evidence suggested that an enzyme called EglN2 plays a role in breast cancer. The data so far from Dr. Kaelin's BCRF-supported research indicate that inactivating EglN2 does not affect normal cells but significantly diminishes the proliferation of human breast cancer cells. This work should motivate the development of drugs that inhibit EglN2.

Bio:
Dr. Kaelin is a Professor in the Department of Medicine at the Dana-Farber Cancer Institute and at the Brigham and Women's Hospital, Harvard Medical School. He obtained his undergraduate and MD degrees from Duke University and completed his training in internal medicine at the Johns Hopkins Hospital, where he served as chief medical resident. He was a clinical fellow in medical oncology at the Dana-Farber Cancer Institute and later a postdoctoral fellow in the laboratory of David Livingston, during which time he was a McDonnell Scholar.

Dr. Kaelin is a member of the American Society of Clinical Investigation and the American College of Physicians. He recently served on the National Cancer Institute Board of Scientific Advisors, the AACR Board of Trustees, and the Institute of Medicine National Cancer Policy Board. He is a recipient of the Paul Marks Prize for cancer research from the Memorial Sloan-Kettering Cancer Center and the Richard and Hinda Rosenthal Prize from the AACR.

A Howard Hughes Medical Investigator since 1998, Dr. Kaelin's research seeks to understand how, mechanistically, mutations affecting tumor-suppressor genes cause cancer. His laboratory is currently focused on studies of the VHL, RB-1, and p53 tumor suppressor genes. His long-term goal is to lay the foundation for new anticancer therapies based on the biochemical functions of such proteins. His work on the VHL protein led to new insights into how cells sense and respond to changes in oxygen, and thus has implications for diseases beyond cancer, such as myocardial infarction and stroke.