Presenter Information

Millie MartinezFollow

Major

Biology

Anticipated Graduation Year

2023

Access Type

Restricted Access

Abstract

Despite significant clinical advances, breast cancer remains the second-leading cause of cancer death in women in the United States. Most tumors are addicted to the hormone estrogen and its transformative genomic effects, through the estrogen receptor (ER), to grow and metastasize. Consequently, ER-targeted hormone therapies (HT) are used to treat and prevent breast cancer metastatic progression. However, prolonged treatment regiments place selective pressure on breast cancer cells, which evolve ER mutations in response. These mutations enable HT resistance, increased metastatic burden, and greatly reduce overall survival. To overcome this resistance, it is crucial to understand how these mutations affect receptor activities. In this study, we measure how clinically relevant and next generation hormone therapies and hotspot mutations affect the formation of an important ER transcriptional complex.

Community Partners

Loyola University Department of Cancer Biology

Faculty Mentors & Instructors

Dr. Sean W. Fanning Ph.D. Department of Cancer Biology, Fr. Peter Breslin Ph.D. Department of Cancer Biology, Kristen Young Department of Cancer Biology

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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Understanding Therapeutic Efficacy in Drug-Resistant Breast Cancer

Despite significant clinical advances, breast cancer remains the second-leading cause of cancer death in women in the United States. Most tumors are addicted to the hormone estrogen and its transformative genomic effects, through the estrogen receptor (ER), to grow and metastasize. Consequently, ER-targeted hormone therapies (HT) are used to treat and prevent breast cancer metastatic progression. However, prolonged treatment regiments place selective pressure on breast cancer cells, which evolve ER mutations in response. These mutations enable HT resistance, increased metastatic burden, and greatly reduce overall survival. To overcome this resistance, it is crucial to understand how these mutations affect receptor activities. In this study, we measure how clinically relevant and next generation hormone therapies and hotspot mutations affect the formation of an important ER transcriptional complex.