Dr. Assaf Hellman

I was born in Eilat on the shore of the Red-Sea and grew up at Kibbutz Yotvata in the Arava valley.  I was a fish farmer until I was 34 when I first joined the Hebrew University of Jerusalem to participate in the "Etgar program for excellent students in Biology".  Due to events in my personal life I realized I would like to make my own mark in current medicine with the advancement of treatments for genetic diseases.

Following the completion of my PhD research under the supervision of Professor Bat Sheva Kerem, I moved to Professor Andrew Chess's lab at the Whitehead Institute at MIT (the Chess lab moved to Harvard Medical School) and started working on the genetics of olfactory receptors in transgenic mice. During this time I became familiar with the genomic studies done at the nearby Broad Institute. Here I began to ponder and investigate the reasons for the apparent failure of the GWAS approach (A genome-wide association study is an approach that involves rapidly scanning markers across the complete sets of DNA, or genomes, of many people to find genetic variations associated with a particular disease.) to explain the variance in individual susceptibility to common human diseases.

It was during this time I decided to take a major change in the direction of my career and began thinking about ways to map genetic-epigenetic variations. This led to the invention of a novel epigenome-wide allele-specific genetic-epigenetic mapping essay (Hellman and Chess, Science 2007). Moreover, my attempts to evaluate the precision of my novel method using the X chromosome as a model led to the discovery of a new genome-wide DNA methylation pattern, now commonly referred to as 'gene-body methylation' in human cells.

I am a faculty member heading a research group at the Hebrew University Faculty of Medicine since 2007. The first goal of my own laboratory was to explore the feasibility of a new research approach towards the genome-wide mapping of diseases contributing epi-variations among large numbers of patients and controls. My unique methodology allows unbiased mapping of the epigenome, thus facilitating the examination of important regions such as distal control elements that are overlooked by the conventional approaches.

Preliminary studies demonstrating the feasibility and efficiency of my approach were recently completed and published (Aran et al 2011, Toperoff et al 2011). These studies provided evidence for predisposing epigenetic variations in Diabetes Type 2, a first report on predisposing methylation variations in T2D.

My long-term objective is to elucidate DNA-based risk factors in the long list of common human diseases, including many metabolic, autoimmune and psychiatric disorders.