- Why Research
- Our Impact
- Get Involved
- About BCRF
- Research is the reason
- Contact Us
You are here
Suzanne A.W. Fuqua, PhD
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.
Metastasis–Stage IV–breast cancer is an incurable disease and the primary cause of breast cancer deaths. Once a breast cancer has reached this advanced stage, it has become resistant to many therapies. Mutations in the estrogen receptor gene (ESR1) are commonly seen in metastatic breast cancer after treatment with aromatase inhibitors (AI). Dr. Fuqua has shown that these mutations not only cause tumors to be resistant to AI, but also driver breast cancer metastasis. Current studies are focused on targeting this unique vulnerability with new anti-cancer drugs.
Full Research Summary
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 3 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.
With 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 drivers of metastasis. These mutations may also make the cells vulnerable to several therapies that are currently used for other indications, such as PARP inhibitors and immune checkpoint inhibitors. In the next year, Dr. Fuqua will test the idea that use of these drugs will effectively treat breast cancers and prevent them from becoming untreatable and life-threatening.
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.