You are here

BCRF Grantee Since

2012

Donor Recognition

The Pink Promises Award in Memory of Patricia L. Hansen

Area(s) of Focus

Myles Brown, MD

Professor of Medicine, Harvard Medical School
Director, Center for Functional Cancer Epigenetics
Dana-Farber Cancer Institute
Boston, Massachusetts

Current Research

Most breast cancers depend on the hormone estrogen for their growth, and therapies that block estrogen are among the most effective and least toxic therapies available. The effectiveness of these therapies, however, is limited to breast cancers that make the estrogen receptor, so-called ER+ breast cancer (ER+). Dr. Brown’s group has found that in addition to female hormones, the male hormones (androgens) acting through the androgen receptor, AR, also play important roles in breast cancer. Depending on breast cancer subtype, androgens can either stimulate or inhibit breast cancer growth. In his current BCRF project, Dr. Brown will leverage information obtained from research in prostate cancer and anti-hormone therapies that have been developed to treat this disease to better understand how androgens work in breast cancer and whether drugs to treat prostate cancer will be effective in some forms of breast cancer. Results from these studies may identify drugs that target AR that can provide the benefits of anti-hormone therapy to increasing numbers of patients.

Bio

Dr. Myles Brown is Director of the Center for Functional Cancer Epigenetics at the Dana-Farber Cancer Institute and Professor of Medicine at Harvard Medical School. He obtained his BS in Biology from Yale and his MD from Johns Hopkins. Following training in internal medicine at the Brigham and Women’s Hospital, a fellowship in medical oncology at the Dana-Farber and postdoctoral research at MIT, he joined the staff of the Dana-Farber and the faculty of Harvard Medical School. Dr. Brown's research is focused on understanding the factors underlying the hormone dependence of breast and prostate cancers. He is recognized for three seminal discoveries including the role of p160 co-activators in steroid receptor action; the dynamic nature of co-regulator function; and the predominance of steroid receptors as enhancer- rather than promoter-binding factors