Eva Y.-H.P. Lee, PhD

2007-2008 BCRF Project:
Recent studies indicate that progesterone, acting through the progesterone receptor (PR), may have a critical role in breast carcinogenesis. Progesterone action is terminated upon PR degradation. Dr. Lee's team has shown that PR degradation is aberrant in BRCA1-deficient mammary epithelial cells. Using a Brca1/p53-deficient breast cancer model, they have shown that anti-progesterone treatment prevents mammary tumor formation. Over the coming year, they will study whether low dose of anti progesterone, mifepristone, and a new generation derivative are effective in preventing/delaying BRCA1-mediated breast cancer, using a well-characterized model system. Functional interactions among BRCA1, PR, and steroid receptor co-activator (SRC) in mammary gland will be studied.

Mid-Year Progress Report:
Progesterone, acting through progesterone receptors (PR), plays a critical role in breast cancer. The breast cancer gene, BRCA1 influences PR stability. Dr. Lee's preliminary studies show that a new anti-progesterone delays tumor formation if given at the right timing. She and her team are using a new system to measure PR activity in the mammary gland to evaluate new anti-progesterone effects.

Bio:
Dr. Lee received her M. Sci. training in developmental biology at National Taiwan Normal University, and Ph.D. training in molecular and cellular biology at the University of California, Berkeley. She was an assistant professor at the University of California, San Diego, and was then promoted to associate professor and professor ranks at the University of Texas Health Science Center at San Antonio. Her team relocated to the University of California, Irvine recently.

Dr. Lee made a significant contribution to our understanding of the first identified tumor suppressor gene, the retinoblastoma (RB) gene, when she was a postdoctoral fellow and a junior faculty member. She played a key role in the isolation of full-length RB gene and provided the first evidence of tissue-specific cell cycle function of RB in vivo.

In recent years, Dr. Eva Lee's lab has been studying how cells respond to DNA damage. Her team identified functional links between cell cycle checkpoint proteins and DNA repair proteins. Mutations of genes encoding these proteins result in cancer predisposition in humans. To better understand breast carcinogenesis and to establish systems for new drug discoveries, her team has established a new mouse mammary tumor model. The new model recapitulates many aspects of human cancer. She has received a Merit Award from NCI to further investigate estrogene receptor expression and oncogene contribution in breast cancer. She is the principal investigator of an NCI-funded mouse consortium project and co-PI of a Department of Defense-funded center of excellence grant.

Dr. Lee plays an active role in serving the scientific communities. She served as chair/co-chair of the NIH study section and workshop. She participated in the USA/Japan meetings, and she will begin to serve as a member of the NCI program project parent committee C this year.