2017 KEYNOTE SPEAKERS
Brenda Andrews is the Charles H. Best Chair of Medical Research, Director of the Donnelly Centre for Cellular and Biomolecular Research and Professor of Molecular Genetics at the University of Toronto. Dr. Andrews’ current research interests include analysis of genetic interaction networks in budding yeast and mammalian cells, using high through-put genetics platforms that include high content microscopy for systematic analysis of cell biological phenotypes. Specific interests in the Andrews lab include mechanisms of cell cycle control, control of cell function by kinases and other enzymes and the regulation of cell polarity and morphogenesis. Her research is currently funded by the Canadian Institutes for Health Research, the National Institutes of Health, the Ontario Research Fund, Genome Canada and the Canadian Institute for Advanced Research (CIFAR). Dr. Andrews is a Companion of the Order of Canada, an elected Fellow of the Royal Society of Canada, the American Association for the Advancement of Science and the American Academy of Microbiology. She was the inaugural Director of the Genetic Networks Program of the CIFAR, and remains a Senior Fellow.
Jean-Pierre Issa is Professor of Medicine and Director of the Fels Institute for Cancer Research and Molecular Biology at Temple University. Dr. Issa's laboratory is involved in both basic and translational research in the field of molecular epigenetics, which refers to stable gene expression states such as X-inactivation, imprinting etc. Specifically, we are interested in epigenetic mechanisms - a DNA modification termed DNA methylation that is commonly abnormal in aging tissues and in various malignancies; and histone modifications involved in determining gene expression states. Current projects include: Large scale mapping of epigenomics patterns in normal, aging and cancer cells; Investigating the causes of aberrant methylation in cancer, focusing on aging; genetic changes; a particular hypermethylator phenotype we described called CpG Island methylator phenotype; environmental exposures and familial predisposition; Basic mechanisms governing the establishment of DNA methylation in normal and cancer cells; Studying the causes and consequences of DNA methylation changes in normal aging tissues; Clinical implications of methylation profiling in cancer and screens for drugs that affect epigenetics.
Our research lies at the interface of technology development and basic science, with a primary interest in studying and eventually programming the processes of organogenesis for regenerative medicine applications. We use human pluripotent stem cells as a core model system, developing and applying methodologies geared towards systematically studying the interplay of gene regulatory networks and cellular niche on normal and aberrant cell fate specification. Given the parallels in phenotypes (such as self renewal and tumor forming ability) between pluripotent stem cells and cancer cells, a key research thrust is also in dissecting aberrant cellular transformation processes such as during tumorigenesis. Towards the above we integrate our core expertise in synthetic biology, genome engineering, and stem cell biology, with instrumentation and materials engineering. The Mali lab's research approach is curiosity-driven, and we are passionate about understanding and progressively engineering biology towards enabling gene & cell based human therapeutics.
Stephen B. Baylin, M.D., is Virginia and D.K. Ludwig Professor of Oncology and Medicine, Co-Director of the Cancer Biology Division and Associate Director for Research Programs of The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. Dr. Baylin's research has contributed heavily to the concept that epigenetically mediated loss of gene function is a major player in the progression of human cancer. Staven Baylin's lab attempts to understand the abnormalities of chromatin and methylation assembly that may account for the appearance of these epigenetic abnormalities during tumor development and how they mediate the transcriptional repression. An interaction between the DNA methylation, histone de-acetylase (HDAC) and histone methylating enzymes mediates the transcriptional silencing. We have also discovered that the enzymes that catalyze DNA methylation, the DNA methyltransferases (DNMTs), are more complex than previously thought and can both inhibit transcription and interact with HDACs, independent of mediating the methylation.