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

UCI Faculty Profile: Eva Lee

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).

List of Publications via PubMed (NIH National Library of Medicine)