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Monday, 28 November 2011

In Body’s Shield Against Cancer, a Culprit in Aging May Lurk

But on Nov. 2, in what could be a landmark experiment in the study of aging, researchers at the Mayo Clinic reported that if you purge the body of its senescent cells, the tissues remain youthful and vigorous.


The experiment was just in mice, and it cleared the cells with a genetic technique that cannot be applied to people. Like all critical experiments, it needs to be repeated in other labs before it can be accepted with confidence.


But the startling result is plausible because it ties together an emerging body of knowledge about senescent cells. And it raises the possibility that attacks on the cells might postpone the diseases of aging and let people live out more of their life span in good health.


Senescent cells were discovered 50 years ago in a classic experiment by the biologist Leonard Hayflick. He found that human cells cultured in glassware do not multiply indefinitely, as was then assumed, but can divide only 50 or so times before lapsing into senescence.


But the finding was not followed up for many years; researchers assumed that it was something that occurred only in the laboratory, or that even if cells did become senescent in the body, there were too few to make a difference.


Only in the last few years have researchers come to realize that senescent cells do occur naturally and that they play central roles in both cancer and aging.


Simple organisms live short lives and do not need cell division. More complex animals live longer because their tissues are renewable. In humans, the cells lining the gut are renewed every five days. Red blood cells last 120 days. Even bone cells slowly turn over, with the result that the entire skeleton is renewed every 10 years or so.


But the price for renewable tissues is cancer: If cells are capable of division, any damage to their control systems can lead to unconstrained growth. The body has therefore evolved two major systems to curb the risk of cancer — cell senescence and cell death.


Both systems are set in motion by illicit cell divisions, like those caused by a virus; by damage to DNA; or by activation of tumor-causing genes. Senescence can also be caused when cells run out of telomeres, the caps at the end of the chromosomes that get shorter at each cell division. This route to senescence, discovered in the 1990s, underlies the process observed by Dr. Hayflick.


Cells thrown into senescence do not divide again but hang about in tissues until they are cleared by the immune system. In cell death, a cell is forced to set off a built-in suicide mechanism.


Researchers do not yet understand why there are two systems, or how the body chooses whether to assign a damaged cell to senescence or to death. But a benefit of senescence is that suspect cells can continue to perform vital functions, said Daniel Peeper, an expert on senescence at the Netherlands Cancer Institute in Amsterdam. Moles, for instance, are collections of senescent cells that continue to produce melanin and defend the skin from ultraviolet rays.


Senescent cells thus seem to be a benign byproduct of the body’s defense against cancer. But researchers have developed growing suspicions of a less benign aspect: the cells’ culpability in aging.


Senescent cells accumulate throughout life, probably because the immune system sweeps them away less efficiently as a person ages. Larger and flatter than normal cells, they are especially common in tissues showing signs of aging, like arthritic knees or the plaque in the arteries.


And despite being termed senescent, the cells are very active: They convert themselves into factories that churn out 100 different kinds of growth factors, along with cytokines, the inflammatory agents that stimulate the immune system. The evolutionary reason for this activity may be to provoke the immune system to attack patches of premalignant and malignant cells.


But the process turns out to have some untoward side effects.

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