New study shows ageing may help prevent cancer growth

A new study led by Stanford University scientists has found that older laboratory mice develop significantly fewer and less aggressive lung tumours than their younger counterparts. The finding challenges the long-standing belief that cancer risk increases with age and mirrors emerging patterns seen in very elderly humans, where cancer rates appear to plateau or even decline.

“It’s a striking finding,” said Associate Professor of Genetics and Pathology, Dr Monte Winslow. “We would expect that older animals would get more and worse cancers, but that’s not at all what the study found. So, what is it about the molecular changes associated with ageing that suppress cancer?”

Factoring in the age element

For decades, scientists have assumed that cancer risk increases steadily with age due to the accumulation of genetic mutations over time. In humans, cancer incidence rises sharply after age 50 and peaks between 70 and 80. Yet, after 85, the risk appears to level off or decline. Researchers have debated whether this drop is due to lower screening rates or biological mechanisms that protect the very old.

In humans, cancer incidence rises sharply after age 50 and peaks between 70 and 80.

The new mouse study suggests the latter. “The standard model of cancer says that as you age, you accumulate bad things in your DNA, and eventually cancer happens,” said Professor Dmitri Petrov, senior author of the study. “But after a certain point, ageing seems instead to act as a general form of cancer suppression.”

Testing cancer across the ages

To explore the relationship between age and tumour development, Dr Emily Shuldiner, a former Stanford graduate student, genetically engineered mice to develop fluorescently tagged lung cancers when exposed to an inhaled gene delivery system. She compared young mice aged four to six months with older mice aged 20 to 21 months – roughly equivalent to humans in their 70s and 80s.

15 weeks after inducing cancer, the younger mice had roughly three times more tumours, which were also significantly larger. “In every way we could measure, the younger animals had worse cancers,” Shuldiner said.

Age alters the impact of tumour-suppressor genes

The study also examined 25 tumour-suppressor genes – genes that normally help prevent cancers from developing. While inactivating these genes increased tumour incidence at all ages, the effect was far greater in younger animals.

One gene that stood out was PTEN. When inactivated, it triggered much stronger cancer growth in young mice compared to older ones. “It suggests that the effect of any given mutation, or the efficacy of therapies targeting that mutation, might differ between young and old people,” Shuldiner explained.

Implications for cancer research and therapy

Further analysis revealed that even in cancer cells from older mice, molecular “signatures of ageing” remained detectable – an unexpected finding given how rapidly cancer cells divide. However, when PTEN was inactivated, these ageing signatures disappeared, making the old cancer cells appear molecularly young again.

Perhaps ageing has a beneficial side that we could harness for better cancer therapies.

According to Winslow, the findings underscore the need to develop cancer models that account for the biological effects of ageing. “For new treatments to be effective, our models need to reflect reality. This study suggests that using only young animals may overlook crucial ageing-related factors,” he said.

Petrov added: “The implications could be huge. Perhaps ageing has a beneficial side that we could harness for better cancer therapies.”