Stephen B. Baylin
Johns Hopkins University
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Primary Section: 41, Medical Genetics, Hematology, and Oncology Membership Type:
Member
(elected 2017)
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Biosketch
Steve Baylin’s laboratory group, for over 30 years has worked to define the origins and role of epigenetic abnormalities in tumorigenesis following their recognition of abnormal gene promoter DNA methylation in cancer in 1986. Their studies include discovering the involved genes and their pathway functions in tumor initiation and progression including Baylin serving as the Co-PI for the epigenetics group in the Cancer Genome Atlas (TCGA) project. From 2000 to 2010, his group identified epigenetically silenced genes co-operating with mutations to over-activate key oncogenic pathways such as the WNT pathway and defined that master regulators of embryonic development constitute the preponderance of genes undergoing promoter hyper-methylation in cancer. Most recently, they are uncovering a link, including recruitment of the protein complexes involved between stress-induced DNA damage integral to cancer risk states and triggering of the above hypermethylation in cancer. Baylin’s team clinically translates their basic findings especially in the context of his role as a co-leader of a Stand Up to Cancer Team. These efforts encompass taking pre-clinically derived basic concepts directly to epigenetic therapy trials for patients and development of correlative biomarkers to predict and monitor therapeutic efficacies. The studies now emphasize that that DNA demethylating agents potentially enhance immune checkpoint therapy through upregulating endogenous retroviral transcripts, triggering an interferon inducing pathway involved with sensing cytoplasmic, dsRNA (“viral mimicry”). This concept now underlies multiple clinical trials aimed at use of epigenetic therapy to improve the efficacy of immune checkpoint therapy for multiple common cancer types.
Research Interests
Dr. Baylin recognized a process of cancer specific, abnormal gene promoter, CpG island DNA methylation associated with epigenetically mediated gene silencing and defined this as an alternative to mutations for producing loss of function for tumor suppressor genes. Baylin was born in Durham, N.C. where he grew up and attended Duke University to obtain his B.A and M.D. degrees. He did his internship in Internal Medicine at Duke and completed his residency for this at Johns Hopkins. He did research training at the NIH in Bethesda, MD as a Staff Associate and Research Investigator from 1969-1971 and did a post-doctoral fellowship in Endocrinology and Physiology at Johns Hopkins from 1972-73. He joined the faculty in the Johns Hopkins Medical Institutions in 1974 and rose to full Professor in the departments of Oncology and Medicine and the Sidney Kimmel Comprehensive Cancer Center in 1986 where he has remained until the present. He holds the Ludwig Professor Chair in Oncology, served as Deputy Director of the Cancer Center from 1992 until 2015 and Associate Director of Research from 2007 through 2015. He is currently co-director of the Cancer Biology Program in the Cancer Center. Dr. Baylin is also a Professor at the Van Andel Research Institute since 2015 and co-Director of a Stand up to Cancer Team for epigenetic therapy. He was elected to the National Academy of Science in 2017.
