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Turning a cellular sentinel into a cancer killer

n less extensive and was not accompanied by apoptosis. Instead the cells underwent cell cycle arrest with features of senescence."

Jacks said that he and his colleagues found no evidence that restoring p53 affected normal cells. "That gives us a broader therapeutic window in which the cancer cells respond rapidly by one of these two mechanisms, whereas normal cells seem to tolerate reactivation of p53 quite well," he said.

In the December 29, 2006, issue of the journal Cell, Gerard Evan at the University of California at San Francisco reported that p53 restoration was effective in killing lymphoma tumor cells.

In a News & Views commentary published in Nature, Norman Sharpless and Ronald DePinho wrote that "these three papers provide reason for cautious optimism that reactivation of p53, and possibly of other tumour-suppressor genes, might be useful in treating certain cancers." However, they noted that Evan and his colleagues had seen rapid appearance of tumors that progressed despite p53 expression, indicating that cancers can mutate to deactivate the pathway or circumvent it.

Both Lowe and Jacks said they agreed that therapies aimed at reactivating p53 would still have to cope with the adaptability of cancers. "For any therapies based on these findings, you would have to imagine that sooner or later, resistance would develop," said Lowe. "And I think the challenge—which is true for any therapy where you can get resistance—is to come up with combination treatments that take out enough of the cancer cells early on that there aren't enough variants left to get around the p53 pathway."

Jacks added that "the main point is that—although there are differences between these mouse models and human cancers—we now can say with some confidence that established tumors are sensitive to p53 reactivation. There are already a number of treatment strategies being tested to restore p53 function, and these might well be expected to hav
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Source:Howard Hughes Medical Institute


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