Michael Kastan
Overview:
Dr. Kastan earned his M.D./Ph.D. from Washington University School of Medicine and did his clinical training in Pediatrics and Pediatric Hematology-Oncology at Johns Hopkins. He was a Professor of Oncology 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 Duke in 2011, where he currently serves as the Executive Director of the Duke Cancer Institute and is the William and Jane Shingleton Professor of Pharmacology and Cancer Biology. His laboratory research has focused on cellular responses to DNA damage, including many highly cited publications reporting the roles of p53 and ATM in DNA damage signaling. Among his numerous honors are election to the National Academy of Sciences, National Academy of Medicine, and the American Academy of Arts and Sciences, and receipt of the AACR-G.H.A. Clowes Memorial Award and Failla Award from the Radiation Research Society. He has served as Chair of the Board of Scientific Counselors of the National Cancer Institute (NCI), on the Boards of Directors of the American Association for Cancer Research (AACR) and the American Association of Cancer Institutes (AACI), and as Editor-in-Chief of the journal Molecular Cancer Research. His lab continues to study molecular and biochemical controls of cellular stress responses, particularly those related to DNA damage, and has spun out two companies focused on novel anti-cancer therapeutics.
Positions:
William and Jane Shingleton Distinguished Professor of Pharmacology and Cancer Biology
Professor of Pharmacology and Cancer Biology
Director of the Duke Cancer Institute
Professor of Pediatrics
Member of the Duke Cancer Institute
Education:
M.D. 1984
Ph.D. 1984
Grants:
Using bacterial CRISPR/Cas endonucleases to selectively eliminate HPV-transformed cells in vivo
Development and Validation of Novel Therapeutic Targets in Anal Cancer
The role of ATM in Metabolic Stress Responses
The role of ATM in Metabolic Stress Responses
Metabolic Sensing and Stress Response Deficit in Ataxia Telangiectasia
Publications:
Participation of ATM, SMG1, and DDX5 in a DNA Damage-Induced Alternative Splicing Pathway.
ATM Regulation of the Cohesin Complex Is Required for Repression of DNA Replication and Transcription in the Vicinity of DNA Double-Strand Breaks.
Abeloff’s Clinical Oncology
Preface
DNA Damage Response Pathways and Cancer
