Stanford researchers report that over a 15-week period older mice developed fewer and less aggressive lung tumors than younger mice, who carried roughly three times the cancer burden and larger tumors. Disabling 25 tumor-suppressor genes highlighted PTEN as having a much stronger effect in young mice. While human implications remain uncertain, the findings mirror a drop in cancer incidence after age 85 and suggest aging can change how mutations and therapies behave.
Stanford Mouse Study Upends Expectations: Younger Mice Develop More and Bigger Lung Tumors Than Older Ones
Stanford researchers report that over a 15-week period older mice developed fewer and less aggressive lung tumors than younger mice, who carried roughly three times the cancer burden and larger tumors. Disabling 25 tumor-suppressor genes highlighted PTEN as having a much stronger effect in young mice. While human implications remain uncertain, the findings mirror a drop in cancer incidence after age 85 and suggest aging can change how mutations and therapies behave.
08:02 AM, 11/14/2025Health
Stanford mouse study challenges conventional thinking about aging and cancer
New experiments from Stanford Medicine found that, over a 15-week observation period, older mice developed fewer and less aggressive lung tumors than younger mice — a result that runs counter to the common expectation that cancer risk steadily rises with age.
The investigators compared groups of mice aged roughly four to six months with mice approaching two years old (about the typical lifespan of a laboratory mouse). Across multiple measures, the younger animals had roughly three times the cancer burden of the older group and developed larger tumors.
“It’s a striking finding,” said Dr. Monte Winslow, associate professor of genetics and pathology. “We would expect that older animals would get more and worse cancers, but that’s not at all what the study found.”
To probe potential mechanisms, the team disabled 25 known tumor-suppressor genes in the animals. One gene in particular — PTEN — produced a markedly stronger effect when inactivated in young mice than in old mice. As former graduate student Dr. Emily Shuldiner summarized: “In every way we could measure, the younger animals had worse cancers.”
Why this matters
Although mice and humans differ in many respects, they share important genetic pathways, including the PTEN gene. In people, PTEN mutations are associated with benign growths (hamartomas) and an increased cancer risk. The new results echo epidemiological observations that cancer incidence can fall after about age 85 in humans, suggesting that aging-related molecular changes might, in some contexts, suppress tumor growth.
Limitations and next steps
The authors caution that these findings are specific to the study design and to mice; the biological mechanisms driving the age-dependent differences remain unclear. Translating results from mouse models to human patients will require additional studies to identify which aging-related molecular or immune changes alter tumor initiation and progression.
The team emphasizes that more research could refine cancer models and influence how targeted therapies are developed and applied across age groups. As biology professor Dr. Dmitri Petrov noted: “The implications of this story could be huge. Maybe aging has a beneficial side to it that we could harness for better therapies.”
Context
For perspective, the American Cancer Society estimates about 226,650 new lung cancer cases and 124,730 deaths in the U.S. this year. Clinicians are also seeing rising rates of some cancers in younger adults — including in never-smokers — a trend attributed to changes in screening, environmental factors, microbiome shifts, and differences in tumor biology across ages.
Bottom line: The Stanford mouse study raises important questions about how age shapes cancer risk and therapy response. While intriguing, these preclinical results should be viewed as a prompt for focused research rather than immediate changes to clinical practice.