
Myles Brown, MD
Professor, Department of Medicine, Harvard Medical School
Physician, Oncology, Brigham And Women's Hospital
Professor of Medicine, Medical Oncology, Dana-Farber Cancer Institute
Contact Info
Myles Brown
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Dana 730
Phone: 617-632-3948
Fax: 617-582-8501
Myles_Brown@dfci.harvard.edu
Administrative Assistant
Medical Oncology
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Dana 730
Phone: 617-582-7646
Fax: 617-582-8501
claudia_steele@dfci.harvard.edu
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Dana 730
Phone: 617-632-3948
Fax: 617-582-8501
Myles_Brown@dfci.harvard.edu
Assistant
Claudia SteeleAdministrative Assistant
Medical Oncology
Dana-Farber Cancer Institute
450 Brookline Avenue
Boston, MA, 02215
Mailstop: Dana 730
Phone: 617-582-7646
Fax: 617-582-8501
claudia_steele@dfci.harvard.edu
DF/HCC Program Affiliation
Prostate CancerBreast Cancer
Research Abstract
Estrogen plays a critical role in the development of the normal breast and in breast cancer. The biochemical mechanisms underlying these processes, however, remain largely unknown. The overall aim of our current research is to build on recent advances in the molecular understanding of estrogen receptor (ER) action to better define the role played by estrogen in the normal breast and in breast cancer. Over the past few years several important coregulatory molecules that play a central role in mediating the transcriptional activity of ER have been identified by several labs including our own. Our current hypothesis is that the differential expression of these molecules accounts in part for the tissue specific activity of selective estrogen receptor modulators (SERMs) such as tamoxifen and raloxifene. In addition, the gene encoding one of these ER coactivators, AIB1, was cloned as a gene Amplified In Breast cancer raising the possibility that altered expression of an ER coactivator may play a central role in estrogen-stimulated breast cancer growth.Our work will provide a better understanding of the role played by alterations in estrogen signaling in breast cancer. Identification of those factors which are markers for these changes are likely to lead to the development of better diagnostic and predictive tools. More importantly, the identification of the factors which are the critical regulators of the alterations in estrogen signaling will become new therapeutic targets and may lead to the development of improved strategies for the prevention and treatment of breast cancer.




