Mutation of the p53 gene is a critical event in the elaboration of many tumors of diverse origin. The p53 protein is activated in response to DNA damage, serving as a checkpoint in the elimination or repair of cells with damaged DNA. Alterations in components of the p53 pathway, such as amplification of the Mdm2 gene, which encodes a p53 inhibitor, also contribute to tumorigenesis. The overall goal of my lab is to understand the signals that regulate the p53 pathway and the consequences of expressing wild-type or mutant p53.
Publications/Creative Works
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Affiliations
Training Grants
NLM Training Program in Biomedical Informatics & Data Science for Predoctoral and Postdoctoral Fellows
Training in Precision Environmental Health Sciences (TPEHS)
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