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For cancer cells, genetics alone is poor indicator for drug response
Date:4/12/2009

initially passed on to progeny, the heritability was transient. The scientists describe it as an extra layer of inheritance, one that is superimposed onto genetic inheritance.

As for what actually causes these protein levels to vary between identical cells, the researchers cited a simple explanation: It's completely random.

"For decades biologists have had this notion that cells produce proteins in orderly, uniform ways, like an assembly line, but they don't," says Sorger. "Rather, cells produce proteins in fits and starts, and the timing and degree varies from one cell to the nexteven cells that are identical in every way. This randomness is something that we're just beginning to appreciate."

These findings also offer an alternative to the cancer stem-cell hypothesis. For that, scientists have posited that certain cancers survive standard treatments because a population of tumor-specific stem cells evades chemotherapy or radiation. This paper, however, offers an alternative explanation, namely, that purely through chance, certain cells produce quantities of proteins that fundamentally alter the cell's response to treatment.

Ultimately, Sorger and his group think that this new insight will make it possible to design anti-cancer treatments that are more effective than those available today.


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Contact: David Cameron
david_cameron@hms.harvard.edu
617-432-0441
Harvard Medical School
Source:Eurekalert

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