These findings, published in the Proceedings of the National Academy of Sciences (PNAS), are the first to show how this chromosomal mutation likely contributes to early development of prostate cancer -- and suggests a model for how other chromosomal translocations, common to many tumor types, are linked to cancer formation and growth.

"This is likely a phenomenon that occurs in many types of cancers when oncogenic fusion genes are over-expressed," says the study's senior author, Dr. Mark A. Rubin, The Homer T. Hirst Professor of Oncology in Pathology and vice chair for experimental pathology at Weill Cornell Medical College.

Dr. Rubin adds that if such an oncogenic protein has the power to throw the switch on thousands of genes, a novel treatment may be able to turn that switch off. "If we understand how this works, then we may be able to borrow that trick to target many genes simultaneously. This discovery would hold a lot of promise for cancer therapy," he says.