Stephen B. Baylin
Visiting Professor of Cancer Epigenetics
- Virginia and D.K. Ludwig Professor of Oncology and Medicine,
- Co-Director of the Cancer Genetics and Epigenetics Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, USA
I have undertaken my research in the Departments of Oncology and Medicine at Johns Hopkins University School of Medicine since 1971 and became a Visiting Professor at the Ludwig Institute for Cancer Research, University of Oxford in 2021.
For over 30 years, I have studied the role of epigenetic gene silencing in the initiation and progression of human cancer. Together with my colleagues, I fostered the concept that DNA hypermethylation of gene promoters, and associated transcriptional silencing, can serve as an alternative to mutations for producing loss of tumour suppressor gene function. We have described some of the classic genes involved, invented approaches to randomly screen the cancer genome for such genes and to demonstrate their functional role in cancer progression, helped begin unravel the molecular mechanisms responsible for the initiation and maintenance of gene silencing, and utilised all of our findings for translational purposes. For the latter activity, I am currently co-leading, with Peter Jones, the Van Andel Research Institute Stand up to Cancer (SU2C) Epigenetic Therapy Team. I have authored or co-authored over 475 full-length publications on the above and other areas of cancer biology.
A combination epigenetic therapy ties blocking MYC to reversing immune evasion and treating lung cancer. Topper MJ et al (2017) Cell 171(6):1284-1300.e21
DNA methylation patterns separate senescence from transformation potential and indicate cancer risk. Xie W et al (2018) Cancer Cell 2018 Feb 12;33(2):309-321.e5
CHD4 Has Oncogenic Functions In Initiating And Maintaining Epigenetic Suppression of Multiple Tumor Suppressor Genes. Xia L et al (2017) Cancer Cell 8;31(5):653-668.e7
Inhibiting DNA methylation causes an interferon response in cancer via dsRNA including endogenous retroviruses. Chiappinelli KB et al (2015) Cell 162, 974–986