Christopher Vakoc

Professor
Cancer Center Program Co-Leader

M.D., Ph.D., University of Pennsylvania, 2007

vakoc@cshl.edu | (516) 367-5045

Cancer cells achieve their pathogenicity by changing which genes are on and off. To maintain these changes in gene expression, cancer cells rely on proteins that interact with DNA or modify chromatin. My group investigates how such factors sustain the aberrant capabilities of cancer cells, thereby identifying new therapeutic targets.

Cancer can be understood as a disease of dysfunctional gene expression control. Research in Chris Vakoc’s lab investigates how transcription factors and chromatin regulators cooperate to control gene expression and maintain the cancer cell state. This work makes extensive use of genetic screens to reveal cancer-specific functions for transcriptional regulators, as well as genomic and biochemical approaches to identify molecular mechanisms. One theme that has emerged from their efforts is that blood cancers are often vulnerable to targeting transcriptional coactivators, such as BRD4 and the SWI/SNF chromatin remodeling complex. Vakoc’s team demonstrated that chemical inhibition of BRD4 exhibits therapeutic effects in mouse models of leukemia, a finding that has motivated ongoing clinical trials in human leukemia patients. The Vakoc lab has also developed a CRISPR-Cas9 screening approach that can reveal individual protein domains that sustain cancer cells. Their lab is now deploying this technology in a diverse array of human cancers to reveal therapeutic opportunities and basic mechanisms of cancer gene control.

Vakoc wins Paul Marks Prize for cancer research
AACR Outstanding Achievement in Cancer Research Award
Forbeck Scholar Award
"V Scholar" by The V Foundation for Cancer Research
Burroughs Welcome Fund Career Award for Medical Scientists
Pershing Square Sohn Prize
Leukemia and Lymphoma Society Scholar Award