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Scientists find a new way to boost common cancer drugs
Date:1/14/2013

uximab. The same was true in mice that lacked this particular pathway, says Astsaturov. "Most tumors are only moderately sensitive to inhibitors of EGFR, but when these tumors lack an essential gene in the cholesterol pathway, they become exquisitely sensitive to the anti-EGFR drugs," he says. "The cancers literally melt away in mice."

The researchers then removed one of the cholesterol genes from the mouse genome, and saw that mice developed patchy, scaly skin. When they biopsied this affected skin, they saw no activity of the EGFR protein, reaffirming that shutting down cholesterol synthesis interrupts EGFR. They also observed the same pattern in normal cell lines.

When the cholesterol biosynthesis pathway is blocked, explains Astsaturov, the normal chain of events that creates a cholesterol molecule is interrupted, and cells accumulate intermediate products of cholesterol that block the normal movement of substances around the cell. This cellular traffic jam makes it difficult for the cell to transport important components, such as EGFR, which has to move between the inside of the cell and its surface to function properly. "If you disrupt this traffic, the cancer cells don't survive."

Eventually, says Astsaturov, researchers can design drugs or look for existing ones that block this cholesterol synthesis pathway. For now, his lab is trying to uncover more details of how the pathway works, the role of each protein that is involvedand whether if, by blocking a protein, they can wipe out tumors in humans that evade current therapies. "These proteins represent targets for additional drugs, which could be combined with EGFR inhibitors," he says.


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Contact: Diana Quattrone
Diana.Quattrone@fccc.edu
215-728-7784
Fox Chase Cancer Center
Source:Eurekalert

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