In cancer fight, cellular suicide may not be the answer

Scientists are examining data that show cellular suicide may not be the answer in the fight to prevent cancer. In fact, studies in mice have found that cell death can sometimes clear the way for cancer to grow, and if these results are confirmed in humans, it could have an impact on cancer drug development. The findings were published recently in Genes & Development.

Research has shown the importance of p53, a protein that acts as a cell's "security system." It works by either halting cell growth, repairing cellular damage, or unleashing Puma, a protein that sets in motion a cell-suicide program called apoptosis, Science News reports.

More than half of all human tumors carry mutations in p53, according to a Nature article. And in studies, mice that lack p53 are riddled with cancer, succumbing to the disease within three months. So researchers had anticipated that mice lacking the Puma protein--and thus the ability to kill damaged cells--would be highly susceptible to cancer after radiation treatment. They therefore tested the ability of mice genetically engineered to lack the Puma protein to withstand repeated rounds of cancer-inducing radiation exposure. And the results were surprising: mice lacking Puma got no tumors at all after repeated rounds of radiation exposure. However, mice with intact Puma developed lymphoma after a couple of rounds of radiation due to overworked stem cells in the bone marrow, Science News notes.

The results are exciting and unexpected, says Lin Zhang of the University of Pittsburgh Cancer Institute in Pennsylvania, as quoted by Nature. And the findings have implications for a class of anticancer drugs designed to mimic PUMA, he adds. "It's a cautionary note," he says. "Those compounds could perhaps cause secondary cancers."

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