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 laboratory is to understand the signals that regulate the p53 pathway and the consequences of expressing wild-type or mutant p53.
Leading the Way in Genetics Research
Lozano elected to Institute of Medicine
Lozano was recognized for her work on the p53 tumor suppressor pathway, specifically in regards to understanding the role of p53 mutants in tumorigenesis and the roles of Mdm2 and Mdm4 as inhibitors of p53. Her fundamental discovery of a transcriptional function for p53 opened the door for new targeted therapies aimed at the p53 mutation. She has developed innovative mouse models, remains the key expert of Mdm2 and Mdm4 in tumorigenesis, and serves as a role model for women and ethnic minorities in science.
Peers elect Lozano as an AAAS Fellow
She earned the distinguished membership in the American Association for the Advancement of Science for her leadership in basic science research and innovative insights into uncovering a type of receptor protein that frequently goes haywire to stimulate cancer growth.