Suzanne A.W. Fuqua, PhD
Professor, Medicine and Molecular and Cellular Biology
Baylor College of Medicine
Overcoming resistance to therapies to prevent metastasis of estrogen receptor-positive breast cancer.
When breast cancer spreads to other tissues, it often loses its sensitivity to anti-cancer drugs. For the most common type of breast cancer, called estrogen receptor (ER)-positive, mutations in the ESR1 gene are a cause of resistance to anti-estrogen therapies called aromatase inhibitors (AI) and promote metastasis. Dr. Fuqua’s research is focused on finding ways to counter the effect of mutated ESR1 in order to improve treatment and prevention strategies for metastatic breast cancer (MBC). Her work could lead to new, more effective ways of managing ER-positive MBC.
Dr. Fuqua and her team previously discovered that mutations in the ESR1 gene are the major drivers in the development of drug resistance leading to metastasis. More recently, they have shown that ESR1 mutations alter cell cycle checkpoints that normally regulate cell growth. Inhibiting these checkpoints in the laboratory significantly blocks metastasis. She and her team have also shown that PARP inhibitors, which target a DNA repair pathway, also block growth of ESR1-mutated tumors. These discoveries could open new therapeutic options for ER-positive patients
In the upcoming year, Dr. Fuqua plans to continue studying the role of cell cycle regulators in resistance to AIs and will test whether cell cycle checkpoint inhibitors combined with endocrine therapy are an effective combination to overcome the effects of ESR1 mutations
Dr. Fuqua has a Bachelor's degree and a Master's Degree from the University of Houston. Her PhD is in Cancer Biology from the University of Texas Graduate School of Biomedical Science. She is a Professor of Medicine and Molecular and Cellular Biology at Baylor College of Medicine. The main goal of her research is to determine the role of specific somatic mutations in estrogen receptor alpha, called K303R and Y537N, in the clinical problem of hormone resistance. Dr. Fuqua was the first to discover alternatively spliced transcriptional isoforms and somatic mutations in breast tumors. She has determined that the K303R mutation alters many aspects of hormone action, including binding to co-regulatory proteins, enhanced stability, estrogen hypersensitivity, response to tamoxifen, and resistance to the aromatase inhibitor anastrazole. Her team discovered the Y537N mutation, a constitutionally active receptor in metastatic tumors. A major goal of her laboratory is to develop novel therapeutics to target these alterations in ER alpha to restore hormone sensitivity, as well as to identify other novel mechanisms of resistance.
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