Lee, Eva Y.-H. P.

EvaLee_120Distinguished Visiting Chair


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EDUCATION AND POSITIONS HELD:

  • B.S., National Taiwan Normal University, 1972
  • M.S., National Taiwan Normal University, 1979
  • Ph.D., University of California, Berkeley, 1984
  • Teaching Assistant, Dept. of Biology, National Taiwan Normal Univ., 1973-1979
  • Research Assistant, Lawrence Berkeley Lab., Univ. of Calif., Berkeley, 1981-1984
  • Post-doctoral Fellow, Dept. of Pathology, Univ. of Calif., San Diego, 1984-1986
  • Postgraduate Res. Biochemist, Dept. of Pathology, Univ. of Calif., San Diego, 1986-1988
  • Assistant Professor in Residence, Dept. of Pathology, Univ. of Calif., San Diego, 1988-1991
  • Asso. Prof., Instit. of Biotech./Ctr. for Mol. Med., UTHSCSA, 1991-1996
  • Professor, Dept. of Mol./Inst. of Biotech., Univ. of TX Hlth. Sci. Ctr., S. A., 1996-2001
  • Professor, Dept. of Biol. Chem. & Dept. of Dev. and Cell Biol., Univ. of Calif., Irvine, 2002-present

HONORS:

  • Predoctoral Fellowship, University of California, Berkeley, 1982-1984
  • Giannini Foundation Postdoctoral Fellowship, 1986-1987
  • Alcon Research Award, 1994
  • Program Director, NCI, Prog. Proj. "DNA Repair and Tumor Suppressor Genes", 2000-2004
  • Program Director, NCI Mouse Consort. Proj. "Mouse Cancer Models by Regulated Inactivation of Tumor Suppressor Genes", 2000-2004
  • NCI Mouse Consort. "Mouse models of human cancer", Breast cancer organ site chairperson, 2000-2004
  • Society of Chinese Biochientists in America Presidential Outstanding Scientist Award, 2001
  • Scientific Director, Avon Breast Cancer Care and Res. Prog., Univ. of Calif., Irvine, 2002
  • Chancellor Professor, Univ. of Calif., Irvine, 2002
  • Academician, Academia Sinica, R.O.C., 2002
  • Breast Cancer Research Foundation Awards, 2003 - present
  • Athalie Clarke Research Award, Univ. of Calif., Irvine, 2008

RESEARCH INTERESTS:

Cell cycle checkpoint pathways and molecular genetics studies of breast cancer using mouse model systems.

Research objective in the Lee laboratory is the understanding of molecular events underlying tumorigenesis. Loss of genome stability is a hallmark of tumor cells that is believed to be important in tumor progression and cancer therapeutic response. Deregulated cell cycle control, failure of cell cycle checkpoint activation, and repair of DNA damage all contribute to loss of genome stability. Study of familial clustered cancers and hereditary cancers in the past two decades has facilitated the identification of tumor suppressor genes whose mutation results in cancer predisposition. Many of these tumor suppressor proteins are involved in these cellular processes.

 

Eva Lee and her laboratory continue to conduct investigations on tissue-specific functions of breast and ovarian cancer susceptibility genes, BRCA1 and BRCA2, and interactions between tumor suppressors and endocrines.
Dr. Lee's group discovered a tissue-specific function of BRCA1 and demonstrated that inhibition of the stabilized progesterone receptor in BRCA1 and p53-mutated mammary epithelial cells prevented or delayed mammary tumors. Her team has continued to focus on the mechanisms of progesterone receptor stabilization as well as the usage of anti-progesterone in breast cancer prevention and progesterone receptor positive breast cancer treatment. How mutations of BRCA genes affect mammary epithelial cell fates and mechanisms of cancer stem cells expansion during the course of chemo-resistance are being studied.

 

In addition, Eva Lee and her laboratory investigate the interaction among checkpoint kinases and DNA repair proteins in the maintenance of genomic stability. Her team demonstrated functional links between ATM and NBS1. They have identified novel mediator, Cep164, for the ATM and ATR signaling pathways that guard genomic stability. How Cep164 network leads to S and G2/M checkpoint activation is being investigated.

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