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Cellular ageing acts like double edged sword in cancers
Washington, Dec 4 (IANS) Cellular senescence or ageing, the process by which biological cells stop dividing in response to stress or damage to their DNA, acts like a double-edged sword.
While it actually prevents cancer in younger persons, it ends up promoting cancer in the elderly.
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.
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Cellular senescence was shown to trigger secretion of proteins that cause inflammation in neighbouring cells and tissue - linked to almost every major disease associated with aging, including many cancers.
Judith Campisi, a cell biologist at 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 tumour suppressor genes slow down the development of cancer, and provides new evidence to support an evolutionary theory about aging.'
Campisi and her colleagues are now developing mouse models through which they can determine whether there are molecular pathways by which senescent cells can either be safely expelled, or selectively destroyed, according to a Berkeley Lab release.
'Senescent cells are extremely stable and do not die, therefore they accumulate in the body over time in multiple tissues,' she said.
The results of this study were published on-line by the Public Library of Science.
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