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Myles Brown, MD
Professor of Medicine, Harvard Medical School
Director, Center for Functional Cancer Epigenetics
Dana-Farber Cancer Institute
Goal: To identify new therapeutic options for patients with estrogen receptor (ER)-positive breast cancer.
Impact: Dr. Brown is using a new gene editing technology to understand why many breast cancers fail to respond to hormonal therapies. His work suggests that male hormones (androgens) may reverse this mechanism of resistance and could lead to new treatments for ER-positive breast cancers.
What’s next: The team will explore drugs that mimic the effects of androgens without the masculinizing side effects of the hormone.
Most breast cancers depend on estrogens (female hormones) for growth, and endocrine therapies that block estrogen action are among the most effective and least toxic breast cancer treatments. Unfortunately, many breast cancers become resistant to them. Dr. Brown has discovered that androgens (male hormones) can either stimulate or inhibit breast tumor growth, depending on breast cancer subtype. He is now investigating whether androgens could reverse resistance to estrogen-blocking therapies.
Full Research Summary
Research area: Improving the effectiveness of therapies for patients with estrogen receptor (ER) positive breast cancer.
Impact: Because most breast cancers depend on the female hormone estrogen for growth, treatments have been developed to prevent the production of estrogen or block its target in cells, the estrogen receptor (ER). However, many ER-positive tumors also express the androgen receptor (AR), which is emerging as a potential biomarker of breast cancer prognosis and therapeutic target. Dr. Brown is investigating whether AR blockers—which have been developed for the treatment of men with prostate cancer—could be an effective treatment strategy for patients whose breast cancers depend on androgens.
Current investigation: He and his team have been using a new gene editing technology to identify why many breast cancers fail to respond to hormonal therapies that target estrogen.
What he’s learned so far: Dr. Brown has found that depending on breast cancer subtype, androgens can either stimulate or inhibit breast tumor growth. His work suggests that AR blockers will be effective in patients whose breast cancers depend on androgens.
What’s next: In the coming year he and his colleagues will explore whether androgens can reverse resistance to hormonal therapies that target estrogens. This avenue of investigation was prompted by their discovery that tumors can become resistant to therapies that inhibit estrogen because of a feedback loop that is activated by blocking estrogen. They believe that this may be prevented with anti-AR therapy.
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.
BCRF Investigator Since
The Pink Promises Award in Memory of Patricia L. Hansen