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Eva Y.-H. P. Lee, PhD
Developmental and Cell Biology and Biological Chemistry
University of California
Seeking to understand how non-cancer cells contribute to the development and progression of BRCA breast cancers.
Laboratory studies are conducted to identify and characterize the early events in BRCA-induced breast cancer and develop targeted prevention strategies.
These novel studies will provide new insight in the prevention of BRCA cancers.
The BRCA1 and BRCA2 genes are the most commonly mutated genes associated with hereditary breast and ovarian cancer risk. Currently, the only preventive strategy is prophylactic removal of the breasts and/or ovaries. The ability to identify early events in the normal breast may provide clues to new prevention strategies as well as early treatments to improve outcomes after cancer diagnosis. Dr. Lee is using a variety of novel laboratory model systems to explore changes in the normal breast of BRCA-mutation carriers that could inform new prevention and treatment strategies for this high-risk group.
Full Research Summary
BRCA1 is involved in many cellular activities including DNA repair, cell cycle checkpoints, and gene regulation, largely by forming different protein complexes. Understanding fundamental facts about BRCA1 functions has led to new therapies for BRCA-related breast cancer as well as possible cancer prevention.
Early detection of changes in the breast before breast epithelial cells become malignant has the potential to improve risk assessment, especially for high risk populations, such as those harboring inherited mutations in the BRCA genes.
Using normal tissue from breast reduction surgery in healthy women, Dr. Lee’s group compared the stromal cells and epithelial cells in BRCA-mutation carriers versus non-mutation carriers. They found early changes in cell compositions as well as molecular alterations in the mammoplasty reduction tissues of the BRCA1 carriers, but not unaffected women.
In the upcoming year, Dr. Lee will use a combination of model systems to identify factors that promote the proliferation of mammary epithelial cells from BRCA1 carriers. They have identified major pathways required for tumor growth and will test which pathways are critical for malignant growth.
These studies will help underscore the molecular factors involved in the heterogeneity of BRCA1-associated breast cancer as well as the identification of potential targets for prevention of BRCA1-driven breast and ovarian cancers.
Eva YHP Lee is the Chancellor’s Professor in the Department of Biological Chemistry at the University of California, Irvine School of Medicine.
In the late 1980’s, Dr. Lee reported the inactivation of the prototypic tumor suppressor gene, the retinoblastoma susceptibility gene (RB), in breast cancer. Subsequently, she and her team investigate how cells repair DNA breaks and identified new players that slow down the cell cycle while DNA damages are being repaired.
Her laboratory has established several breast cancer models to address the breast-specific function of the breast cancer susceptibility gene, BRCA1. They found that BRCA1 plays a role regulating the levels of progesterone receptors (PR). Her team has investigated the mechanisms involved and addressed whether anti-progesterone could be used to delay mammary tumors using the model systems. In addition, Dr. Lee and her team are exploring the link between the circadian system, BRCA1 and the regulation of female hormones.