Chancellor’s Professor & Chair
Department of Biological Chemistry
University of California, Irvine
In 2012-2013, Dr. Lee shifted her research focus from microRNAs to circadian rhythm and breast cancer development and found that a central circadian player, period 2, repressed the expression of a group of genes critical for tumor progression. Circadian rhythms, commonly referred to as our body’s “internal clock,” are known to influence many physiological and biological functions, and there may be correlations between disruption of circadian clocks and cancer formation. Earlier studies suggest that variants in a family of genes, called PER, which are responsible for regulating the body’s circadian rhythm, may increase an individual’s risk of developing breast cancer. Dr. Lee’s team will continue their study to see how alterations in PER genes may influence breast cancer progression, as molecular mechanisms of PER genes deregulation in tumorigenesis are not well understood. In addition, her team will continue to examine how metabolic alterations may affect the onset of breast cancer, specifically how circadian disruption affects tumorigenesis in BRCA1 and p53 laboratory models.
Dr. Lee’s studies indicate that disruption of circadian influences the level of circulating progesterone as well as the expression and activities of progesterone receptor in the BRCA1 breast cancer model. Tumor progression is also affected by circadian disruption.
Dr. Lee received her master's of science training in Developmental Biology at National Taiwan Normal University and PhD 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 where she is now Chancellor's Professor.
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 laboratory model of mammary tumor. The new model recapitulates many aspects of human cancer. She has received a Merit Award from National Cancer Institute (NCI) to further investigate estrogen receptor expression and oncogene contribution in breast cancer. She is the principal investigator of an NCI-funded 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.