Cellular senescence a double-edged sword( Scientists have identified a molecul...),Health

Scientists have identified a molecular cause behind the ravages of old age and in doing so have also shown how a natural process for fighting cancer in younger persons can actually promote cancer in older individuals. Cellular senescence, the process by which biological cells stop dividing in response to stress or damage to their DNA, was shown to trigger the secretion of proteins that cause inflammation in neighboring cells and tissue. Inflammation is linked to almost every major disease associated with aging, including many cancers.

Judith Campisi, a cell biologist who holds a joint appointment with the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) and the Buck Institute for Age Research, led this research.

"In this study, we provide for the first time a broad molecular description of how cellular senescence, which is well known as a mechanism for cancer prevention, also drives aging and age-related disease by changing the local tissue environment," she said. "Our study also defines a new paradigm for how oncogenes promote and tumor suppressor genes slow down the development of cancer, and provides new evidence to support an evolutionary theory about aging."

The results of this study were published on-line by the Public Library of Science (PLoS) in a paper entitled: "Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor."

Co-authoring the paper with Campisi were Jean-Philippe Copp and Christopher Patil, members of Campisi's research group in Berkeley Lab's Life Sciences Division, Joshua Goldstein, now with the Novartis Research Foundation; Francis Rodier and Denise Muoz of the Buck Institute; and Peter Nelson and Yu Sun from the Fred Hutchinson Cancer Research Center in Seattle.

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