Scientists Offer Insight Into Roots of Age, Cancer

UC Berkeley researchers are taking a closer view at a scourge that all people in time become familiar with–the inexorable advent of age.

Aside from wrinkles, aging creates increased risks for a host of diseases, including cancer.

Although aging is inevitable, it is not a well-understood process.

"We want to understand the molecular and cellular basis for aging and hopefully, find out what we can do about it," said Judy Campisi, a scientist at Lawrence Berkeley National Laboratory.

Campisi and other scientists have proposed that both aging and cancer are related to a process called cellular senescence, in which cells irreversibly stop dividing.

Senescence is the body's quick-fix against cancer, because cells that cannot divide cannot form tumors.

"There are cells in your body that will never divide, like neurons and muscles," Campisi said. "You never get cancer from those cells."

However, when a quick-fix falls apart, the consequences are often dire.

"We have data now to support that the senescence response prevents cancer in young organisms, but may actually promote cancer late in life," Campisi said.

Senescent cells have long-term negative effects by virtue of their dysfunctional actions.

"(A senescent cell) becomes dysfunctional in two ways: one is that it doesn't perform its normal function; the other is that it begins to secrete molecules (that) can eventually destroy tissue," Campisi said.

The secreted molecules include substances that degrade elastic tissue, promote inflammation and stimulate growth in neighboring cells, possibly promoting cancer if these cells are precancerous.

If her hypothesis proved correct, Campisi hoped to reduce the risk of cancer by eliminating senescent cells.

Campisi had an explanation for why the body opted for senescence at the possible expense of long-term health–for the vast majority of human history, people have had short lives.

"Anything that was optimized to keep us healthy for the first thirty years of age could have bad effects after 60 or 70, but evolution could never select against that," Campisi said.

Although the hypothesis that senescent cells promote cancer and aging is unproven, Campisi said that it was gaining credibility.

"I think, most scientists in the field, including me, believe that it's a reasonable explanation for the age-related increase in cancer," said Jan Vijg, a physiology professor at the University of Texas Health Science Center in San Antonio (UTHSCSA).

Paul Hasty, a molecular medicine professor at UTHSCSA, urged more research before targeting senescent cells for destruction.

"Before we can realistically think of medical intervention we need to understand aging much better than we do," Hasty said.

More research will certainly aid medical efforts to turn back time.

"We are clearly on our way to inhibit age-related deteriorative effects," Vijg said. "The more we learn about causes of aging, the easier it will be to make more of such drugs."

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