Cigall Kadoch, PhD, Epigenomics Program Co-Director at the Broad Institute of MIT and Harvard

Overview of Recording

This is an exciting time in biomedical research. Exome- and genome-wide sequencing studies have provided unprecedented new insights into the molecular—and, specifically, genetic—underpinnings of human disease. For the first time, we are identifying the genes that drive cancer, neurologic disease and many other conditions. Dr. Cigall Kadoch’s research seeks to translate these human genetic discoveries into biochemical mechanisms and new opportunities for therapeutic development.

This webinar focuses on the efforts of Dr. Kadoch and her team on the regulation of our genome’s architecture and how disturbances in this system can cause disease. It also provides perspectives into how industry and academia can partner in pursuit of innovation and entrepreneurial opportunities.

About the Presenter

Cigall Kadoch, Ph.D. is an Assistant Professor of Pediatric Oncology at the Dana-Farber Cancer Institute, Affiliate Faculty of Biological Chemistry and Molecular Biology at Harvard Medical School, and Institute Member and Epigenomics Program Co-Director at the Broad Institute of MIT and Harvard. She is also the scientific founder of Foghorn Therapeutics in Cambridge, MA.

She established her independent laboratory in 2014, at age 28, one of the youngest scientists ever appointed to the Harvard Medical School faculty, immediately following completion of her Ph.D. studies in Cancer Biology at Stanford University working with developmental biologist Gerald Crabtree. She has quickly become a leading expert in chromatin and gene regulation and is internationally recognized for her groundbreaking studies in these areas. Specifically, her laboratory studies the structure and function of chromatin remodeling complexes such as the mammalian SWI/SNF (or BAF) complex, with emphasis on defining the mechanisms underlying cancer-specific perturbations. Of note, the recent surge in exome- and genome-wide sequencing efforts has unmasked the major, previously unappreciated contribution of these regulators to malignancy: genes encoding subunits of mammalian SWI/SNF complexes are mutated in over 25% of human cancers.