Eva Y.-H. P. Lee
Ph.D., University of California, Berkeley, 1984
Dept. of Biological Chemistry & Dept. of Developmental and Cell
Biology
University of California, Irvine
Room 128, Sprague Hall
Irvine, CA 92697
Office: (949) 824-9766
Lab: (949) 824-9767
elee@uci.edu
Research Interests:
Cell cycle checkpoint pathways and molecular genetics studies of breast cancer using mouse model systems
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 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.
Selected Publications:
Zhao, S., Yuan, F. S.-S., Weng, Y.-C., Lin, Y.-T., Hsu, H.-C.,
Lin, S.-C. J., Gerbino, E., Song, M.-H., Zdzienicka, M. A., Gatti,
R., Shay, J., Ziv, Y., Shiloh, Y. and Lee, E.Y.-H.P.
A functional link between ATM kinase and NBS1 in the DNA damage
response. Nature, 405: 473-477 (2000).
Post, S., Weng, Y-C., Cimprich K., Chen, L. B., Xu Y., and
Lee, E.Y.-H.P. Phosphorylation serines 635 and 645 of human
Rad17 is cell cycle regulated and is required for G1/S checkpoint
activation in response to DNA damage. Proc. Natl. Acad. Sci.
USA, 98: 13102-13107 (2001).
Lin, S.-C. J., Lee, K.-F., Nikitin, A., Hilsenbeck, S. G., Cardiff,
R. D., Li, A., Kang, K.W., Frank, S.A., Lee, W.-H.,and Lee,
E.Y.-H.P. Somatic mutations of p53 lead to ER(-positive and
negative mouse mammary tumors with high frequency of metastasis.
Cancer Res., 64: 3525-32 (2004).
Poole*, A., Li*, Y., Kim, Y., Lin, S.-C. J., Lee, W.-H. and
Lee, E. Y.-H. P. Preventionof BRCA1-mediated mammary
carcinogenesis by anti-progesterone. Science
314:1467-1470 (2006).*equal 1st authors
Furuta, S., Wang, J.-M., Wei, S., Jeng, Y.-M., Jiang, X., Gu, B.,
Chen, P.-L., Lee, E. Y.-H.. P. and Lee, W.-H.
Removal of BRCA1/CtIP/ZBRK1 repressor complex on ANG1 promoter leads
to accelerated mammary tumor growth contributed by prominent
vasculature. Cancer Cell, 10: 13-24 (2006).
Lee, E. Y.-H. P. Promotion of BRCA1-associated
triple-negative breast cancer by ovarian hormones. Curr.
Opin. Obstet. Gynecol. 20: 68-73 (2008).
Sivasubramaniam, S., Sun, X., Pan, Y., Wang, S., and Lee,
E.Y.-H.P. A novel mediator protein, Cep164, is requiredfor
the maintenance of genomic stability through modulation of MDC1,
RPA, and CHK1. Genes & Dev. 22: 587-600 (2008).
Shafee, N., Smith, C.R., Wei, S., Kim, Y., Mills, G., Hortobagyi,
G.N., Stanbridge, E. J., and Lee, E. Y.-H. P.
CD29hi24+ cancer stem cells contribute to cisplatin-resistance in
Brca1/p53-mediated mouse mammary tumors. Cancer Res.
68 (9): 3286-94 (2008).
