Day 2 :
Oncology Fox LLC, USA
Keynote: Leading the global collaborative effort in epigenetics through a next generation search engine and portal for the oncology community
Time : 9:30 AM - 10:15 AM
David A Ligon is the founder & CEO of Oncology Fox LLC. David established a global collaborative network of Education Technology Leaders. David Ligon brings more than 30 years of experience in Information Technology to the table, with a focus on Web and Systems design as well as Technical Documentation, Education, Grants and Leadership. Given David's passion for cutting-edge research and technology, it was only natural his direction would evolve in life to combine all these gifts into Epigenetically focused and Knowledge Management-based Cancer Research Portal of the 21st Century to foster communication and collaboration in the industry--all with the Goal of Saving Lives through Awareness and Knowledge-sharing.
Online networking and knowledge-sharing through application of the principles of knowledge management in development of the next generation cancer research portal is leading the global collaborative eff ort in epigenetics. Th e paradigm has fundamentally and profoundly changed in recent years on how we approach the understanding of cancer treatment and its latest breakthroughs. So much funding has been funneled to Cancer research that there is a big data problem coordinating and sharing those results. Further, Cancer research itself has outgrown previous search portal models in that they do not understand nor apply the principles of epigenetics or knowledge management to searching and sharing information. Top trophy announcements oft en get buried in the news, knowledge of new diagnostic markers, targeted therapies, clinical trials and CRISPR advances are not properly knowledge-shared. Oncology Fox addresses these problems in addition to providing a way for advanced cancer therapies service providers to market their wares to a targeted audience. Developing a sense of community amongst stakeholders fi rst is a key in achieving the level of collaboration needed globally to lead and forge a direction for epigeneticists in our common mission. Th e goal is to save lives through awareness and collaboration. By applying the principles of knowledge management toward a next generation cancer research portal and establishing a new content indexing and validation methodology for collaborative knowledge sharing in the 21st century we can achieve these goals. Th e global collaborative eff ort has pulled together the top researchers, doctors, institutions, donors and the infi rmed to provide a complete solution.
Chiba University, Japan
Keynote: Induction of epigenetic alterations in gastric epithelium and their contribution to gastric tumorigenesis
Time : 10:15 AM - 11:00 AM
Atsushi Kaneda has obtained his MD degree from University of Tokyo and became Assistant Professor at the Department of Gastrointestinal Surgery, University of Tokyo where he conducted genome-wide DNA methylation analysis in gastric cancer and acquired PhD degree. He has also studied at Johns Hopkins University and showed that accumulated epigenetic alteration could modify intestinal tumor risk using mouse model of IGF2 LOI. As an Associate Professor at University of Tokyo and as Professor at Department of Molecular Oncology, Chiba University since 2013, he has conducted projects to clarify epigenomic mechanisms in gastrointestinal carcinogenesis.
Cancer arises through accumulation of epigenetic and genetic alterations and therefore is stratifi ed into several molecular subtypes using comprehensive epigenomic and genomic information. We showed that accumulated epigenomic alteration could causally modify tumor risk. We also comprehensively stratifi ed gastric cancer into 4-5 DNA methylation epigenotypes, depending on pathogens. While the majority of gastric cancer is associated with Helicobacter pylori infection, a subset of gastric cancer, ranging 7-15%, is associated with Epstein-Barr virus (EBV) infection. EBV+ gastric cancer exhibits most severe DNA hypermethylation and EBV itself was shown to cause the extensive hypermethylation phenotype when infected into gastric epithelial cells, involving increased expression of DNMT1. Demethylating enzyme TET2 was found to function as a resistant factor against DNA methylation induction and hMeDIP-seq and MeDIP-seq analyses revealed that target regions of hydroxy methylation by TET2 signifi cantly overlapped with target regions of de novo DNA methylation by EBV infection. Th e repression of TET2 due to viral transcripts or up-regulated human miRNAs signifi cantly contributes to de novo methylation acquisition. Other epigenomic alterations are also involved in promoter regions, enhancer regions, etc., during EBV infection and cause aberrant regulation of critical genes e.g. proliferative genes or tumor suppressor genes. Another cancer subtype with DNA hypermethylation phenotype involves aberrant methylation of mismatch repair gene MLH1, leading to microsatellite instability (MSI) and gene hypermutation in gastric cancer. Th ese subsets of gastric cancer with hypermethylation phenotype, i.e., EBV+ subtype and MSI-high subtype, showed unique gene mutation patterns, which contribute to gastric tumorigenesis synergistically with DNA hypermethylation.