Functional genomics and epigenomics of complex disease genetics

2 Nov 2012

Manolis Kellis
Department of Computer Science and Engineering, MIT, and
The Broad Institute of Harvard and MIT


Most disease-associated variants for complex disease lie in non-coding regions, have weak effects, and remain functionally uncharacterized. Genome-wide functional genomics datasets provide the opportunity to build regulatory models that seek to interpret how these contribute to the disease phenotype. In this talk, I will present our efforts to integrate genomic variation, epigenomic variation, and functional genomics datasets with genome-wide association studies to understand the molecular basis of complex disease.

Our results suggest a general framework for integrating multi-cell functional genomics and epigenomics information to decipher cis-regulatory connections in complex disease.

current theory lunch schedule