Elsa R. Flores , Ph.D. 1999, University of Wisconsin-Madison UT M. D. Anderson Cancer Center Molecular and Cellular Oncology Contact Information

Research Interests: Tumor suppressor genes, DNA damage, apoptosis, gene expression, transcriptional regulation, mouse genetics

The research in my laboratory is focused on understanding the p53 family of genes. We are interested in understanding the functions of the newest p53 family members, p63 and p73. These genes are more structurally complex than p53 and are involved in many cellular functions including the DNA damage response, apoptosis, and tumor suppression.

A tutorial in my laboratory would include using an in vivo approach to understanding the p53 family of genes in transcriptional regulation of target genes. The student will gain experience in mouse genetics and anatomy, tissue culture, and transcriptional assays.

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E.R. Flores, S. Sengupta, R. Bronson, D. Crowley, J.B. Miller, J. Newman, A. Yang, F. McKeon, and T. Jacks. 2004. Tumor predisposition in mice mutant for p63 and p73: evidence for broader tumor suppressor functions for the p53 family. Cancer Cell. manuscript submitted.

E.R. Flores, S. Sengupta, and T. Jacks. 2004. Genes involved in DNA repair are transcriptional targets of p63 and p73. manuscript in preparation.

E.R. Flores, K.Y. Tsai, D. Crowley, S. Sengupta, A. Yang, F. McKeon, and T. Jacks. 2002. p63 and p73 are required for p53-dependent apoptosis in response to DNA damage. Nature 416:560-4, 2002.

E.E. Reczek, E.R. Flores, A.S. Tsay, L.D. Attardi, and T. Jacks. 2003. Multiple response elements and differential p53 binding control PERP expression during apoptosis. Mol Cancer Re s. 1(14):1048-57, 2003 .

A. de Vries, E.R. Flores, B. Miranda, H.M. Hsieh, C.T. van Oostrom, J. Sage, and T. Jacks. 2002. Targeted point mutations of p53 lead to dominant-negative inhibition of wild-type p53 function. Proc Natl Acad Sci USA 99(5):2948-53, 2002.