Epigenetics and epigenetic networks offer a novel and potentially groundbreaking platform for predictive analytics and biomarker discovery. Epigenetic analytic solutions extend beyond existing genomic technologies and represent a more predictive and dynamic biomarker discovery framework as compared to genomics because, unlike genomic biomarkers, epigenetic marks change very rapidly in response to environmental changes, drug therapies, and in disease. The dynamic and rapid epigenetic changes in response to a variety of stimuli allows early detection of patient responses to drug therapies as well as detection of early stages of disease. The first portion of the presentation will highlight my ideas for the potential applications of artificial intelligence technologies to characterize disease-specific epigenetic networks. The second portion of my talk will introduce exosomal histones as universal liquid biopsy-based epigenetic biomarkers and potential therapeutic targets relevant in immune-dysfunctional conditions such as rheumatoid arthritis and inflammatory bowel disease as well as inimmuno-oncology.
Roman Alpatov is a Clinical Genomics Variant Scientist at IBM Watson. He obtained his Ph.D. degree at the University of Florida, where he independently developed a new concept describing a novel function of the splicing regulator Pinin in the regulation of transcription. In addition, using a transcriptional co-repressor CtBP as a model, Roman introduced a new paradigm, such as simultaneous regulation of a tumor suppressor gene activity through the coordinated action at transcriptional and splicing proteins. After obtaining his Ph.D. degree, Roman pursued his postdoctoral training at Harvard Medical School, where he studied epigenetics of fragile X syndrome. He described for the first time the role of fragile X mental retardation protein FMRP in DNA damage response at the chromatin interface, a significant finding which will hopefully open new avenues in treatments of this disorder. Specifically, he found that FMRP binds methylated chromatin, a previously unknown feature of this molecule, and regulates DNA damage response in a chromatin-dependent manner. These findings offer an entirely new paradigm in fragile X field, where FMRP participates in the nuclear events in addition to its classical role as a translational regulator in the cytoplasm. Roman also introduced a potential role for FMRP in metastatic cancer.