Senior citizens, rejoice.

While getting older has long been linked to higher cancer risk, new research suggests that after a certain age, the odds don’t just plateau — they may actually drop.

“The implications of this story could be huge,” Dr. Dmitri Petrov, senior author of the paper and a biology professor at Stanford University, said in a statement. “Maybe aging has a beneficial side to it that we could harness for better therapies.”

Traditionally, cancer rates climb sharply after 50, hitting their highest point between the ages of 70 and 80.

“The standard model of cancer is, with age you accumulate bad things in the form of mutations,” Petrov explained. “When you collect enough bad things, cancer happens.”

You might assume that would make cancer almost inevitable at a certain age, but that isn’t the case. Around 85, the curve flattens even starts to drop.

“After a certain point, aging appears instead to be a generic form of cancer suppression,” Petrov said.

Why this happens has long been a mystery — but now, scientists might finally have some clues.

In the study, Stanford researchers compared mice aged four to six months, roughly equivalent to young adulthood in humans, with mice 20 to 21 months old, when most molecular signs of aging are present.

But these weren’t ordinary rodents. The mice had been genetically engineered to develop fluorescent lung tumors when exposed to a special inhaled gene delivery system.

After triggering tumor formation, the scientists waited 15 weeks before examining the animals’ lungs again.

They found that the young mice had three times more cancer than the older ones. The young mice also had about three times as many tumors, which were significantly larger than those in their older peers.

“It’s a striking finding,” Dr. Monte Winslow, senior author of the study and an associate professor of genetics and of pathology at Stanford, said in a statement.

“We would expect that older animals would get more and worse cancers, but that’s not at all what the study found,” he continued. “So, what is it about the molecular changes associated with aging that suppress cancer?”

Hoping to find out, the team switched off 25 tumor-suppressor genes in the mice. These genes, many linked to normal aging, produce proteins that help block cancer development.

When tumor formation was triggered again, the effects of disabling these genes were weaker in the older mice.

In other words, while tumor incidence rose in mice of all ages with inactivated tumor suppressors, the increase was far greater in the younger animals — especially for one gene in particular.

“PTEN inactivation stood out as having a much stronger effect in young mice,” Dr. Emily Shuldiner, a former graduate student and lead author of the paper, said in a statement.

“It suggests that the effect of any given mutation, or the efficacy of cancer therapies targeted at specific mutations, might be different in young versus old people,” she continued.

That’s significant, because because most mouse cancer studies to date have focused on younger animals.

“We develop these animal models of cancer with an eye to developing new treatments for patients,” Winslow said. 

“But for this to work, the models have to be correct. And this study suggests that models using young animals may not be accurately reflecting important aging-related changes.”

By studying older mice, researchers hope to better understand how aging protects against cancer — and potentially use that knowledge to help humans.

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