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K-Ras' Achilles' heel

Three research teams associated with Harvard Medical School have identified key proteins and pathways that K-Ras-driven tumors require for survival, providing points to disrupt the proliferation of cells that harbor drug-resistant mutations of the oncogene. These secondary targets include a bevy of kinases and other enzymes involved in cell division.

Many of these weak spots in the underlying wiring of K-Ras (KRAS)-driven tumors are already being pursued by cancer companies. Indeed, the new studies suggest that rather than being an unwanted complication, K-Ras activation may in fact increase the sensitivity of tumors to drugs that target these secondary pathways.

K-Ras activation often occurs in non-small cell lung cancer (NSCLC), colon cancer and pancreatic cancer, and it leads to poor prognosis and response to therapy because of aggressive tumor growth. Previous studies had suggested that tumors with K-Ras mutations acquire other genetic alterations,1 but the importance of these other pathways for tumor survival was poorly understood.

"Most of the focus on targeting K-Ras-positive tumors has been the K-Ras pathway," said Jeffrey Settleman, professor of oncology at Massachusetts General Hospital. "These new studies point out that we can go beyond

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