Professor, Medicine and Molecular and Cellular Biology
Baylor College of Medicine
Seeking to reduce resistance to anti-estrogen therapies and prevent breast cancer metastasis.
Studies are ongoing to understand the mechanisms by which mutations in the estrogen receptor gene promote breast cancer metastasis.
These studies are advancing our understanding of drug resistance and metastasis and will inform the development of better treatment and prevention strategies.
Around 20-30 percent of all breast cancer cases will become metastatic, and the number of women currently living with metastatic breast cancer in the US is estimated to be over 155,000. Unfortunately, the median survival after a metastatic breast cancer diagnosis is only three years.
Dr. Fuqua's work is focused on understanding how mutations in the estrogen receptor gene (ESR1) influence breast cancer metastasis. Since her initial discovery of ESR1 mutations in breast cancers, her laboratory has remained at the forefront of efforts to delineate the functional mechanisms associated with their emergence in metastatic tumors by applying genomic and molecular technologies to this clinical problem.
Due to the advent of liquid biopsies (looking for cancer cells in blood), metastatic patients can be monitored during targeted therapies. As a result, the incidence of detected ESR1 mutations in metastatic patients has risen significantly, with current estimates up to 40 percent.
Dr. Fuqua's team has shown that ESR1 mutations are not just a mechanism of resistance to hormone treatment, but are a major driver of metastasis. In the next year, Dr. Fuqua will continue to examine the mechanisms associated with ESR1 mutant-driven metastatic growth.
These studies will increase our understanding of the complex cellular interactions between the most common ESR1 mutations and breast cancer metastasis and ultimately inform the development of new strategies to effectively treat metastatic cancer.
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.