Guillermina Lozano

The University of Texas MD Anderson Cancer Center


Election Year: 2017
Primary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type: Member

Biosketch

Guillermina (Gigi) Lozano is a geneticist recognized for her studies of the p53 tumor suppressor pathway, from characterizing p53 as a transcriptional activator to characterizing the physiological importance of Mdm2 and Mdm4 proteins as inhibitors of p53. Lozano was born in East Chicago, Indiana before moving to Texas with her family where she completed undergraduate studies in Biology and Mathematics at Pan American University. She completed graduate studies at Rutgers University and the University of Medicine and Dentistry of New Jersey, and a post doctoral fellowship at Princeton University. She was hired as an Instructor at The University of Texas MD Anderson Cancer Center in 1987 and rose through the ranks to her current position as chair of the department of Genetics. She was elected a Fellow of the American Association for the Advancement of Science. She received the Minorities in Cancer Research Jane Cooke Wright Lectureship, and Women in Cancer Research Charlotte Friend Lectureship awards both from the American Association for Cancer Research. Dr. Lozano is also the recipient of distinguished alumni awards from both her undergraduate and graduate alma maters. She is a member of the National Academy of Sciences and the National Academy of Medicine.

Research Interests

Gigi Lozano directs a research laboratory that studies the p53 tumor suppressor pathway in vivo using mouse models. Her laboratory characterized the function of p53 as a transcriptional activator which laid the foundation for numerous studies on transcription functions and targets of p53. They also determined the physiological importance of Mdm2 and Mdm4 proteins as inhibitors of p53 activity and further probed this exquisite relationship showing that minor changes in Mdm2 levels via polymorphisms directly impact cancer risk. Her laboratory further demonstrated the importance of the Mdm proteins in regulating p53 in numerous cell types including stem cells. Mouse models with p53 missense mutations firmly established the gain-of-function phenotype of a common p53 mutation and its mechanism of action, while a separation-of-function p53 mutant showed that the ability to induce cell cycle arrest and senescence (in the absence of apoptosis) are also tumor suppressive functions of p53. Her laboratory also showed that mutant p53 is inherently unstable similar to wild type p53, but is stabilized in tumors by DNA damage signals. Lastly, a therapeutic model highlights the unexpected finding that breast tumors with mutant p53 respond better to treatment with DNA damaging agents.

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