Professor, Department of Oncology
Co-Leader Breast Cancer Program
Lombardi Comprehensive Cancer Center
Understanding the relationship between obesity, inflammation, and breast cancer risk after menopause.
Obesity increases the risk of breast cancer after menopause and is associated with a worse outcome in breast cancers diagnosed at any age. Dr. Slingerland is studying how obesity and post-menopausal estrogens increase breast cancer risk and promote estrogen receptor (ER)-positive breast cancer progression to a more aggressive disease. Her work may reveal new strategies for preventing the disease from developing and spreading beyond the breast.
Dr. Slingerland and her team have found that signaling through the estrogen receptor appears to cooperate with obesity-induced inflammation signaling, particularly after menopause. They observed that when fat cells interact with breast cancer cells in the breast tissue, an inflammatory reaction occurs in both the cancer and fat cells that drives tumor progression. She and her team have found that estrone, the main estrogen produced after menopause, contributes to inflammation in the breast and drives its metastatic progression. In the last year, they showed that pre- and post-menopausal estrogens are not equivalent: pre-menopausal estrogens exert protective effects while post-menopausal estrone is a potent driver of breast cancer development and progression. Furthermore, estrone cooperates with the transcription factor NFkappaB to facilitate metastasis.
In the upcoming year, Dr. Slingerland will test how pre- and post-menopausal estrogens interact with the ER and NFkappaB to induce or repress gene programs relevant to breast cancer. She and her team will also study how estrone, the estrogen that dominates after menopause, might stimulate tumor metastasis by helping cancers evade anti-tumor immunity. This work may identify novel, estrone-activated gene drivers of breast cancer in obesity and determine whether estrone interferes with the anti-tumor immune reaction that would normally be activated to destroy cancer cells.
Joyce Slingerland, MD, PhD is currently Professor in the department of Oncology and co-Leader of the Breast Cancer Program at Lombardi Comprehensive Cancer Center, Georgetown University. Prior to moving to Georgetown, she was a professor in the Department of Biochemistry and Molecular Biology at the University of Miami, as well as a member of the senior leadership of the University of Miami Sylvester Comprehensive Cancer Center (UMSCCC) and Co-Program Leader of the UMSCCC’s Molecular Oncology and Experimental Therapeutics Program. She has published over 70 articles and reviews in addition to several book chapters and has received numerous awards.
Dr. Slingerland received her MD from the University of Toronto in 1983, followed by a Fellowship in Internal Medicine with the Royal College of Physicians and Surgeons in Canada. In 1987, she was certified by the American Board in Internal Medicine and in Medical Oncology by the Royal College of Physicians and Surgeons. In August of 2002, Dr. Slingerland came to the University of Miami School of Medicine as the Director of the Braman Breast Cancer Institute, Sylvester Comprehensive Cancer Center, where she is working to expand and coordinate research efforts on breast cancer from many disciplines.
Dr. Slingerland discovered the “cell growth brakes” molecule p27 and her research investigates how cancer cells lose growth restraints. Current work also investigates the causes underlying resistance to endocrine (also called anti-estrogen) therapies for breast cancer. She is also focused on why obesity increases breast cancer risk and worsens patient outcomes and is testing effects of a fatty environment on breast cancer stem cells.
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