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Researchers find roadmap to next-generation cancer therapies
Date:5/25/2008

es responding synergistically to cooperating oncogenic mutations might act as the drivers toward malignancy, Land said. It now appears that this hunch has paid off.

Spear-headed by co-authors Helene R. McMurray, Ph.D., a post-doctoral fellow, and graduate students Erik R. Sampson, George Compitello and Conan Kinsey, the team found that among 30,000 cellular genes, only about 100 genes responded synergistically to the combination of two of the most prevalent cancer genes, Ras and p53, and were expressed differently in normal and cancer cells.

Accordingly, the research group termed these 100 genes CRGs, for cooperation response genes. By studying a subset of the CRGs, researchers also found that 14 of 24 CRGs were essential to tumor formation. In contrast, only one of 14 genes responding in a non-synergistic manner (non-CRGs) had a similar effect.

The significance of Ras and p53, and by association the CRGs, is enormous. Ras and p53 are implicated in about half of all cancers. When p53, a tumor-suppressor gene, loses its function, and when Ras becomes hyperactive, both genes play major roles in promoting uncontrolled growth of colon, pancreas and lung cancers.

Ras activation and p53 loss-of-function cooperatively work together through the CRGs, which encode proteins that regulate cell signaling, cell metabolism, self-renewal, cell differentiation and cell death.

Indeed, CRGs may provide us with a surprisingly large and valuable set of targets for interventions that will destroy cancer cells and leave normal cells unharmed, Land said. We are very excited with the results.


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Contact: Leslie Orr
Leslie_Orr@urmc.rochester.edu
585-275-5774
University of Rochester Medical Center
Source:Eurekalert

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