CEWG Seminar Series
To join the Cancer Evolution Seminar Series, email AACR staff.
October Cancer Evolution Seminar
October 7, 2021
11:00 am – 12:30 pm EDT
Jeff Townsend, Yale School of Public Health
Vincent Cannataro, Emmanuel College
David McCandlish, Cold Spring Harbor Labs
September Cancer Evolution Seminar
September 2, 2021
11:00 am – 12:30 pm EDT
Jason Somarelli, PhD
Assistant Professor Department of Medicine
Director of Research, Duke Comparative Oncology Group
Duke Cancer Institute
Jason Somarelli is an Assistant Professor of Medicine and Director of Research for the Duke Comparative Oncology Group. His research focus is on studying the mechanisms of cancer therapy resistance and metastasis through the lens of comparative evolutionary and ecological paradigms.
Gábor Balázsi, PhD
Henry Laufer Professor, The Louis and Beatrice Laufer Center for Physical & Quantitative Biology
Professor, Department of Biomedical Engineering
Stony Brook University
Title: Mapping the landscapes of chemoresistance and metastasis
Abstract: Various steps in chemoresistance or metastasis can be conceptualized as cells exploring fitness landscapes, such as cell survival or invasiveness as a function of gene expression. I will illustrate the utility of fitness landscapes in understanding chemoresistance and metastatic processes and provide examples of how we can infer such landscapes experimentally with the help of noise-controlling synthetic gene circuits in human cancer cells.
Gábor received his undergraduate Physics degree in 1996 at the Babeş-Bolyai University in Cluj/Kolozsvár, Romania. In 2001 he completed a Physics PhD in noise-induced spatiotemporal dynamics at the University of Missouri at Saint Louis. From 2002 – 2005, as a Systems Biology postdoctoral fellow at Northwestern University in Chicago, he studied gene-regulatory network response to environmental perturbations. From 2005 – 2006, as a Synthetic Biology postdoctoral fellow at the Center for Biodynamics at Boston University, he developed synthetic gene circuits to study how cellular diversity promotes drug resistance. As Assistant and then Associate Professor at the University of Texas MD Anderson Cancer Center, from 2006 – 2014 his team built a growing library of expression-controlling synthetic gene circuits in yeast and human cells. He was a recipient of the 2009 NIH Director’s New Innovator Award, which aims to “stimulate highly innovative research and support promising new investigators”. Since 2014 and 2020, as the Henry Laufer Associate Professor and then Professor of Physical and Quantitative Biology at Stony Brook University, he and his team developed and experimentally evolved synthetic gene circuits, advancing the understanding of gene network evolution, drug resistance and cancer progression. His research is part-experimental and part-computational, fostering interdisciplinary training while advancing the frontiers of quantitative biology.
James DeGregori, PhD
Courtenay C. and Lucy Patten Davis Endowed Chair in Lung Cancer Research
Dpt. of Biochemistry and Molecular Genetics
University of Colorado Anschutz School of Medicine
Title: Aging, somatic evolution, and cancer – the inexorable link
Abstract: Why do we get cancer? Why is cancer highly associated with old age? Of course, aging is associated with the accumulation of more mutations, and some of these mutations can contribute to cancer phenotypes. But we now understand that carcinogenesis is much more complex than originally appreciated. In particular, there are tissue environmental forces that both impede and promote cancer evolution. Just as organismal evolution is known to be driven by environmental changes, somatic evolution in our bodies is similarly driven by changes in tissue environments, whether caused by the normal process of aging, by lifestyle choices or by extrinsic exposures. Environmental change promotes selection for new phenotypes that are adaptive to the new context. In our tissues, aging or insult-driven alterations in tissues drives selection for adaptive mutations, and some of these mutations can confer malignant phenotypes. We have been using mouse models of cancer initiation, mathematical models of cellular evolution, and analyses of human tissue samples to better understand the evolutionary forces that control somatic cell evolution and thus cancer risk. We will discuss how our studies together with the myriad of recent analyses of clonal evolution in normal tissues informs a new understanding of links between aging and cancer.
James is a Professor in the Department of Biochemistry and Molecular Genetics (faculty since 1997) and Deputy Director of the University of Colorado Cancer Center. He has degrees from the University of Texas at Austin (BA Microbiology) and the Massachusetts Institute of Technology (PhD Biology), and received postdoctoral training at Duke University. His lab studies the evolution of cancer, in the context of their Adaptive Oncogenesis model, with a focus on how aging, smoking, Down Syndrome, and other insults influence cancer initiation and responses to therapy.