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The Ras pathway in cancer therapy

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If you have a question about this talk, please contact Kate Davenport .

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K-Ras genes and N-Ras are frequently activated in cancer. Attempts to develop drugs that target mutant Ras have so far been unsuccessful. The reasons for these failures, and possible solutions based on new approaches, will be discussed. Drugs that inhibit Raf have failed to show clinical benefit in Ras-mutant tumors. In contrast, they paradoxically induce the Raf MAPK pathway in these cells. This, we propose, is because Raf is negatively regulated by auto-phosphorylation, so that Raf inhibitors relieve auto-phosphorylation before they inhibit MEK phosphorylation. K-Ras is activated far more frequently than N-Ras or H-Ras in human cancers. K-Ras, but not H-Ras activates a set of genes which are involved in stem cell phenotypes,. K-Ras is able to promote multiple stem cell characteristics in vitro and in vivos. These data may explain why cancer cells driven by K-Ras are especially difficult to treat and offer new opportunities for therapeutic intervention

This talk is part of the Cancer Research UK Cambridge Institute (CRUK CI) Seminars in Cancer series.

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Average on Saturdays: 7448.29411765 kWh In person - location TBC via zoom, meeting ID 940 1803 7756

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