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January 4, 2011
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Old Age and Cancer


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American Cancer Society

The Biology of Aging and Cancer



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Growing older might be inevitable, but why does it bring a huge increase in cancer risk? As this ScienCentral News video reports, genetics researchers studying yeast have found evidence of a switch that triggers cancer with aging.

Why Study Yeast to Get to the Bottom of Cancer?

Yeast don't get cancer, but aging yeast cells do get something a lot like it. "They too have one of these hallmarks of cancer, they get chromosomal instability, the chromosomes get all mixed up near the end of their life," says Daniel Gottschling, a researcher at the Fred Hutchinson Cancer Research Center and professor of genome sciences at the University of Washington.

Gottschling and his colleague Michael McMurray measure the age of a yeast by counting its offspring, called daughter cells, which appear white. They genetically manipulated the yeast cells to change color from white to red if there were abnormal chromosomes, a sign of genetic instability. They saw a lot more red when the yeast hit middle age, suggesting there's an age-linked switch for cancer. Studying this switch in yeast could help scientists solve the link between aging and cancer.





Why is Cancer Considered a Disease of Aging?

Although it can strike both young and old, cancer is primarily considered a disease of aging. In the United States in 1900, the average lifespan was 48 years old and 3.7% of total deaths were caused by cancer. By 1997, the average lifespan increased to over 76 years, with 23.3% of total deaths caused by cancer. Fifty percent of all malignancies and 67 percent of cancer deaths occur in persons over the age of sixty-five. "In the first 30 or 40 years of your life you normally don't have any cancer," says Gottschling, "but suddenly as you hit your 50s the incidence of cancer begins to go up astronomically.

"There have been a lot of hypotheses to try to explain the phenomenon of why do humans get cancer as they get older," he says. "Unfortunately, because there are so many hypotheses out there, and because we live so long, it's been difficult to figure out which of the hypotheses is actually true."





In Gottschling's lab, genetically manipulated yeast cells changed from white to red if there were abnormal chromosomes.
One hypothesis is that cancer, caused by the accumulation of mutations that ultimately produce a cell capable of uncontrolled growth, so that older people are more vulnerable to cancer because they've been exposed to carcinogens— pollution, tobacco, sun, radiation, alcohol, bad diet, and maybe even stress— longer.




"It is tempting to think that cancer occurs later in life because of a steady accumulation of mutations," David Sinclair, pathology professor at Harvard, wrote in an accompanying commentary to Gottschling's research, which was published in Science. "Certainly, cells isolated from the elderly have more chromosomal abnormalities than cells from the young. But the story is not so simple because rates of spontaneous mutation are too low to account for the extensive genome rearrangements found in tumors."

Another hypothesis is that genetic mutations that can lead to cancer tend to occur more frequently in older people. "Experiments in mice have confirmed the suspicion that mutation rates increase with age. The molecular basis of this increase in mutation rate is still under debate," wrote Sinclair.

The DNA repair system in a healthy body is constantly on the lookout for dangerous changes that may cause a cell to become cancerous, and aborts the cell when it finds such mutations. This system is not as effective as people get older. This could be because "genes required for preventing or repairing DNA damage are mutated, leading to runaway DNA instability," wrote Sinclair. "Although this is probably a major part of the story, some researchers argue that it fails to explain fully the gross chromosomal abnormalities and tissue distribution of most adult cancers."

"One idea that's consistent with our results, is that there is something being built up over time in cells," says Gottschling. "One of the hypotheses was that DNA was being damaged over time, and essentially we hit a threshold and all heck breaks loose. Well, from our data, it doesn't look like it's that simple, but rather than maybe oxidative damage is occurring over time to something else. The something else, we think, is proteins that are important in making sure that the chromosomes remain intact and don't get damaged."

"With the discovery that we've made, where we see this basically equivalent of a cancer-like phenomenon in yeast cells, this now gives us some focus into which of those hypotheses might actually be true, and even more so, it gives us the potential to test the hypotheses and eventually [create] either drugs or modes of treatment if what we see in yeast is true in humans as well."

This research was published in the September 26, 2003 issue of Science and was funded by the National Science Foundation (NSF), the National Institutes of Health (NIH) and Ellison Medical Foundation.


 
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