Guillermina (Gigi) Lozano
The University of Texas MD Anderson Cancer Center
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Primary Section: 41, Medical Genetics, Hematology, and Oncology Membership Type:
Member
(elected 2017)
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Biosketch
Dr. Lozano received her BS degree in Biology and Mathematics, Magna Cum Laude, from Pan American University now the University of Texas Rio Grande Valley. She received her PhD from Rutgers University and the University of Medicine and Dentistry of New Jersey, and performed post-doctoral studies with Dr. Arnold Levine at Princeton University. Dr. Lozano was hired as an Instructor at The University of Texas MD Anderson Cancer Center in 1987 and quickly rose through the ranks to her current position as professor and chair of the department of Genetics. Dr. Lozano is a member of the National Academy of Sciences, the National Academy of Medicine and the American Academy of Arts and Sciences. She received the Minorities in Cancer Research Jane Cooke Wright Lectureship and the Women in Cancer Research Charlotte Friend Lectureship awards, both from the American Association for Cancer Research. She also received the EE Just Award from the American Society of Cell Biology. She is also the recipient of distinguished alumni awards from both her undergraduate and graduate alma maters.
Research Interests
Dr. Lozano's research is focused on understanding the activites of the p53 tumor suppressor and the upstream signals that regulate p53 function. Dr. Lozano identified Mdm2 and Mdm4 as critical inhibitors of p53, the relevance of an Mdm2 single nucleotide polymorphism on cancer risk, the importance of the Mdm2 feedback loop in DNA damage response, and the impact of elevated Mdm4 levels on tumorigenesis. Dr. Lozano generated models that identified gain-of-function mechanisms for p53 missense mutations which result in more aggressive cancers. Other models showed that cell cycle arrest and senescence (independent of apoptosis) were important p53 tumor suppressive mechanisms and explored the clinical implications of restoring p53 activity in different contexts in vivo. Restoration of p53 causes tumor regression in the absence of p53 but only suppresses tumor growth in tumors with amplified Mdm2 setting the stage for combination therapies. These studies led to an expanded and deep understanding of the mechanisms that drive tumorigenesis and their response to therapies. Development of a new somatic mouse model that generates p53 missense mutations in a few cells has explored p53 mutations as drivers of tumor development and evolution in the context of a normal stroma and immune system.
