Scott W. Lowe is a cancer geneticist known for work on tumor suppressor gene networks and their action in cancer suppression and therapy responses. His work has made important contributions to our understanding of the roles and regulation of p53 in apoptosis or senescence and in characterizing and exploiting mechanisms by which cancer gene mutations alter therapy responses. He obtained his Bachelors of Science Degree in Biochemistry from the University of Wisconsin-Madison and his Ph.D. from the Department of Biology in the Massachusetts Institute of Technology. In 1995, he initiated independent research as Cold Spring Harbor Laboratory Fellow, where he rapidly transitioned to an Assistant, then Associate Investigator. He was named Full Professor in 2000 and became an Investigator of the Howard Hughes Medical Institute in 2005. In 2011, he moved his laboratory to the Memorial Sloan Kettering Cancer Center, where he currently serves as Chair of the Cancer Biology and Genetics Program in the Sloan Kettering Institute and oversees the Geoffrey Beene Center for Cancer Research. He has received several awards including the Outstanding Investigator Award from the American Association for Cancer Research, the Paul Marks Prize, and the Alfred G. Knudsen Award, and is a member of the American Academy of Arts and Sciences and the National Academy of Sciences.

Research Interests

Scott Lowe's laboratory studies tumor suppressor gene action in order to identify key regulatory nodes controlling basic cellular processes and to reveal the strategies nature uses to combat cancer. They also interrogate the genes and processes that drive cancer, explore how they interact to produce distinct tumor phenotypes, and attempt to identify cancer specific vulnerabilities for targeting therapeutically. Their approach combines mouse models, genetic tools, and cancer genomics in a coordinated manner that allows them to study cancer gene networks in a comprehensive way. Current projects in the laboratory focus on p53 action and the consequences of various p53 mutations, the roles and regulation of cellular senescence in cancer and aging, and how loss of function mutations in tumor suppressor genes sustain tumor maintenance. They also are developing powerful genetic approaches and non-germline mouse models to accelerate the pace at which cancer genes can be studied in vivo, and are using functional genomics to interrogate oncogenic mechanisms and identify new therapeutic targets.

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Primary Section

Section 41: Medical Genetics, Hematology, and Oncology