Michael B. Kastan

Duke University

Primary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type:
Member (elected 2016)


Michael Kastan earned MD and PhD degrees from Washington University and did his clinical training in Pediatrics/Pediatric Hematology-Oncology at Johns Hopkins. He was a Professor of Oncology, Pediatrics and Molecular Biology at Johns Hopkins prior to becoming Chair of the Hematology-Oncology Department and later Cancer Center Director at St. Jude Children’s Research Hospital, before moving to become Executive Director of the Duke Cancer Institute in 2011. His laboratory has focused on DNA damage signaling and his discoveries have made a major impact on our understanding of both how cancers develop and how they respond to chemotherapy and radiation therapy. His publications reporting the roles of p53 and ATM in DNA damage signaling are among the most highly cited publications of the past twenty-five years. Honors for his work include election to the National Academy of Sciences, the National Academy of Medicine, and the American Academy of Arts & Sciences, and receipt of the AACR-G.H.A. Clowes Memorial Award for outstanding contributions to basic cancer research. He has served as Chairman of the Board of Scientific Counselors of the National Cancer Institute and on the Boards of Directors of the American Association for Cancer Research and the American Association of Cancer Institutes.

Research Interests

Damage to cellular DNA contributes to cancer development and is a mechanism by which many cancer therapeutics work. My laboratory has focused on understanding the mechanisms by which cells recognize and repair damage to their DNA and on the cellular signaling pathways that determine the cellular and organismal outcomes after DNA damage. We made the seminal observation that the tumor suppressor gene product, p53, is a central mediator of cellular responses to DNA damage and a major determinant of cell viability after DNA damage and other stresses. We subsequently demonstrated that DNA damage activates the ATM protein kinase and initiates a complex signal transduction pathway that includes the induction and phosphorylation of p53 protein. This signaling pathway is now called the “DDR” or DNA Damage Response pathway. Several participants in this signaling pathway have turned out to be important determinants of cancer susceptibility and we, and others, are now targeting some of these molecules to improve outcomes after cancer therapy. Interestingly, several of these molecules are also turning out to have functional roles outside of DDR signaling, such as in regulation of metabolic signaling, thus almost certainly impacting on physiological processes in addition to cancer.

Powered by Blackbaud
nonprofit software