|Awarded On||August 20, 2014|
|Title||Collateral Genomic Deletions as Targetable Vulnerabilities in Cancer|
|Award Mechanism||Individual Investigator|
|Institution/Organization||The University of Texas M.D. Anderson Cancer Center|
|Principal Investigator/Program Director||Ronald DePinho|
|Cancer Sites||All Sites|
One way a normal cell becomes a cancer cell is by deletion of genes that normally prevent uncontrolled cell proliferation, termed tumor suppressor genes (“drivers”, as in drivers of cancer formation). Because the deletion of such tumor suppressor genes occurs stochastically, these deletions often include additional neighboring genes, that do not directly play a role in regulating cell growth, and in many instances, play important roles in cell metabolism (deletion of genes which does not directly contribute to cancer progression are termed “passenger”). Because most critical metabolic processes are carried out by multiple related genes, loss of single one can be readily tolerated by in-built...