Harvard Medical School
Emil Frei III Professor of Medicine
Director, Center for Functional Cancer Epigenetics
Dana-Farber Cancer Institute
Improving immunotherapy in triple-negative breast cancer.
Triple-negative breast cancer tumors do not have estrogen, progesterone, or HER2 receptors commonly found in breast cancer. While traditional chemotherapy and newly developed immunotherapies are successful in treating some patients with TNBC, it is an aggressive breast cancer subtype, and many patients succumb to the disease. This is partly driven by the fact that TNBC tumors are very heterogeneous, so no single therapy will be effective for all patients.
Dr. Brown has been working to find new and effective treatments for TNBC including combination targeted therapies and immunotherapy. His work on immune response to TNBC grew out of studies aimed at understanding the detrimental effects of obesity on TNBC outcomes. Researchers currently don’t know how obesity-driven changes to breast fat tissue regulate the immune response in TNBC. The goal of his work is to understand the mechanism by which obesity suppresses anti-tumor immunity, with the hope of improving immunotherapy in TNBC.
Dr. Brown and his team are using laboratory models to study fat and tumor cells on the single-cell level. His team has shown that obesity promotes cancer growth in laboratory models and markedly increases a specific type of macrophage – a type of immune cell – in fat tissues. Their studies further showed that in the presence of obesity, TNBC tumor cells produce proteins that attract macrophages. Based on these findings, they hypothesize that obesity causes the recruitment of these macrophages to the tumor, and then suppress the anti-tumor immune response in TNBC.
In the coming year, the team will work to define the relationship between macrophages, obesity, the immune microenvironment and TNBC tumor growth and progression. Elucidating this mechanism will help the team and other researchers target the ability of tumor cells to attract tumor promoting macrophages or reverse the obesity-induced macrophage activity to improve the response of TNBC to immunotherapy.
Myles Brown, MD is Director of the Center for Functional Cancer Epigenetics at Dana-Farber Cancer Institute (DFCI) and Emil Frei III Professor of Medicine at DFCI and Harvard Medical School. He obtained his BS in Biology from Yale and his MD from Johns Hopkins University School of Medicine. 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 Cancer Institute 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. He is a member of the National Academy of Medicine, the National Academy of Sciences and Fellows of the American Academy of Cancer Research (AACR), the American Academy of Arts and Sciences, and the American Association for the Advancement of Science (AAAS). He is on the Editorial Board of the Proceedings of the National Academy of Sciences.
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