Research on Cancer Gene Poses a Dilemma Three separate research teams agree: A gene that prevents cancer also accelerates aging. The gene plays a role in preventing cells from dividing. That's good if they're cancer cells, but bad if they're healthy cells that need replenishing.
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Research on Cancer Gene Poses a Dilemma

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Research on Cancer Gene Poses a Dilemma

Research on Cancer Gene Poses a Dilemma

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ROBERT SIEGEL, Host:

From NPR News, this is ALL THINGS CONSIDERED. I'm Robert Siegel.

MICHELE NORRIS, Host:

And I'm Michele Norris.

While listening to the following story, you are going to age approximately four minutes, but researchers may have a way to take some of the sting out of getting older. Today, three scientific teams say they found one of the reasons people age.

As NPR's Joe Palca reports, scientists probably won't be able to stop aging, but they may be able to slow the unpleasant consequences of getting older.

JOE PALCA: Norman Sharpless of the University of North Carolina in Chapel Hill has been searching for genes related to aging. He focused on an anti-cancer gene called p16. Anti-cancer genes put the brakes on cell proliferation, so cells don't divide uncontrollably and form tumors. But he wondered whether the gene was also preventing aging organs from renewing themselves.

So Sharpless asked what would happen if you took p16 away? He created a strain of mice that didn't have the anti-cancer gene. Sure enough, the mice without p16 kept healthy, young-looking organs filled with young looking cells even as they grew older. But they didn't live any longer than normal mice.

NORMAN SHARPLESS: The good news is, you don't age as quickly. The bad news is you get cancer. I like to think of this as the James Dean phenomenon, you know, of live fast, die young and leave a good-looking corpse.

PALCA: Not necessarily a good solution to the aging problem. But remember, even if p16 didn't make the animals live longer, it did make their cells behave like they did when they were young. And that gives scientists a way of studying how cells behave when they age normally, and what changes when they age missing p16. Sean Morrison took up that challenge. He focused on what happens to stem cells.

SEAN MORRISON: You have stem cells in many different tissues that are required to generate new cells every day.

PALCA: Morrison is a stem cell biologist at the University of Michigan in Ann Arbor.

MORRISON: You have stem cells in your bone marrow that make new blood cells every day, stem cells in your skin that make new skin cells, even stem cells in your brain that make new brain cells. And we've always known that during aging that tissues have less capacity to grow and less capacity to repair themselves after injury.

PALCA: In the current issue of the journal Nature, Morrison reports that brain stem cells missing p16 don't appear to age. They retain their capacity to grow and repair injury.

In a second paper, stem cell biologist David Scadden shows that blood stem cells also retain their youthful vigor when p16 is missing. Scadden is director of the Center for Regenerative Medicine at Massachusetts General Hospital in Boston. He says even though p16 isn't the answer to living longer, tinkering with someone's p16 levels may make it possible to treat traumatic injuries.

DAVID SCADDEN: We'll have to be very careful with the way this gene is regulated. But if we can modify it following a particular kind of injury, you might be able to enhance the restoration of function, and that would be a very, very powerful tool.

PALMER: There's another way p16 might be useful in medicine. North Carolina's Norman Sharpless, who has the third Nature paper on p16, says scientists know that p16 levels go up as humans age. But they may go up at different rates in different people. So maybe you're only as old as your molecules say you are.

SHARPLESS: You know, there's molecular age, and then there's chronologic age. And as a physician, I can tell you that some patients who say they're 60 look a lot older, and some patients who say they're 70 look quite spry.

PALCA: Sharpless says the more spry, the better they can tolerate certain drugs. Now the three new studies all seem to show that the same genetic change that makes cells stay youthful also makes you more susceptible to cancer. But Cynthia Kenyon isn't convinced that's always true.

Kenyon is director of the Hillblom Center for the Biology of Aging at the University of California San Francisco. She's been studying animals with genetic mutations that make them live longer.

CYNTHIA KENYON: And what we did was we asked, okay, what happens to tumors in these animals? And we found that all of these different genes that extend lifespan also delay tumors.

PALCA: So there's a chance someday we'll all live longer, cancer-free lives. And, by the way, you're now four minutes and 17 seconds older exactly.

Joe Palca, NPR News, Washington.

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