Research published in today's online version of Nature sheds light on why certain cancer cells die (apoptosis) in response to chemotherapy, while others stop proliferating (citostasis) and try to repair the damaging effects of the drug. For years, scientists have tried to understand what determines this choice - citostasis versus apoptosis -in order to influence that decision in favor of cell death during the course of treatment.

Researchers at Memorial Sloan-Kettering Cancer Center demonstrated that cancer cells containing a high level of a protein called Myc cannot activate the production of the p21 gene, which inhibits cell division. According to the study's authors, Myc binds to p21 and blocks its ability to stop cell proliferation, creating conditions that allow the cancer cells to die off.

"Our work reveals a way we might coax cells to favor apoptosis instead of citostasis in order to increase the effectiveness of chemotherapy," said Howard Hughes Medical Institute Investigator Joan Massague, PhD, Chairman of the Cell Biology Program at Memorial Sloan-Kettering and senior author of the study. "Now, time and more research need to reveal how feasible this strategy would be in the clinic."

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CITATIONS

Nature, Oct-2002 (Oct-2002)