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A Study in RAF: On-Target Effects Can be Surprisingly Fickle

This article was originally published in Start Up

Executive Summary

Two independent research teams have shown that current RAF inchibitors, a class of experimental targeted cancer drugs, may only work well in patients with one particular mutation - in an enzyme called BRAF. In other people, the drugs can actually contribute to the growth of tumors. The findings echo develoments earlier in the decade with EGFr inhibitors, which proved to be harmful to some patients until the mechanism of action was worked out and their use subsequently restricted.

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A New Genetic Connection In Liver Cancer -- As Powerful As Her2/neu In Breast?

New data point to a targeted strategy for treating a significant subset of liver cancers and importantly, provide a biomarker for identifying patients who could benefit from the therapy. It's based on the discovery of a correlation between amplification of a growth factor gene and overexpression of the gene's protein product -- a phenomenon that mirrors the way in which amplified Her2/neu gene expression promotes a subset of breast cancer, which led to the development of Herceptin.

Reversible Drug Resistance in Tumor Cells

Cancer patients sometimes respond more than once to treatment with the same agent even after resistance develops, supporting the notion that reversible, non-genetic mechanisms may be at work. A group at Massachusetts General Hospital recently identified such a mechanism in non-small-cell lung cancer and has started to trace its origins. They have linked this phenomenon to HDAC and IGF-1 receptor pathway - already known druggable targets - suggesting the potential for combination therapies that could extend the efficacy of some cancer drugs.

Teasing Out Mechanisms of Small-Molecule Kinase Inhibition

Even as kinases remain a popular target in oncology for industry, two recent papers show how much we have yet to learn about how to interfere with these molecules. These most recent laboratory studies help explain the confusing observation that the very act of inhibiting a kinase with a drug can also "prime" phosphorylation of that target, which in some cases can actually enhance tumor activity.

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