Disrupting a cancer gene
Scientists at Harvard-affiliated Dana-Farber Cancer Institute have successfully disrupted the function of a cancer gene involved in the formation of most human tumors by tampering with the gene’s “on” switch and growth signals, rather than targeting the gene itself. The results, achieved in multiple myeloma cells, offer a promising strategy for treating not only myeloma but also many other cancer types driven by the gene MYC, the study authors say. Their findings will appear in the print issue of the journal Cell on Sept. 16. Details of the study are currently available on the journal’s website. “Cancer is a disease of disregulation of growth genes in a cell, and MYC is a master regulator of these genes,” says James E. Bradner of Dana-Farber and Harvard Medical School (HMS). Bradner is one of the study’s senior authors. Previous attempts to shut down MYC by inhibiting it directly with drug molecules have been notably...