For decades, low-dose aspirin has been investigated as a possible cancer-preventing agent. Observational studies and meta-analyses have suggested regular users may see a 20–30% reduction in colorectal cancer risk, but large randomised clinical trials have painted a more complex picture.
One of the biggest of these, the ASPREE trial, tested daily low-dose aspirin (100 mg) in more than 19,000 healthy older adults (aged 70+, or 65+ for US Black and Latino participants). Over almost five years of follow-up, aspirin did not reduce overall cancer incidence compared with placebo.
So is the cancer-prevention story for aspirin over? Not quite.
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A Closer Look with “Effect Score” Analysis
Instead of relying on one-size-fits-all subgroup comparisons (which often lack statistical power), researchers applied an effect score model. This approach estimates each person’s individualized treatment effect (ITE) — essentially, whether aspirin is more likely to help or harm you based on your unique characteristics.
In this secondary ASPREE analysis, published in JAMA Oncology, of 9,350 participants (median follow-up 4.5 years), 1,009 (10.8%) developed cancer and 195 (2.1%) died. Aspirin was predicted to be beneficial for about 59% of the population, harmful for about 41%. Predicted ITEs ranged from −23.0% to 21.5%, with a median 5-year absolute cancer risk improvement of 2.3% (IQR 0.7%–3.7%) when comparing the model to a treat-all strategy.
Key factors shaping aspirin’s impact included:
- Smoking status – Current smokers were more likely to experience harm from aspirin.
- Clonal hematopoiesis of indeterminate potential (CHIP) – Participants with CHIP (a common age-related genetic change in blood cells) at a higher allele frequency (≥10%) were more likely to benefit.
- Other predictors – Older age, family history of cancer, and lower body mass index (BMI) leaned toward benefit. Meanwhile, higher BMI, diabetes, polypharmacy, and a prior cancer history leaned toward harm.
Why CHIP Matters
CHIP has recently emerged as a marker of increased risk for both blood and non-blood cancers, as well as cardiovascular disease. In this study, CHIP status was one of the strongest predictors of who might benefit from aspirin.
There’s a plausible biological link: CHIP has been tied to elevated inflammatory signals like IL-6 and TNF-α. Aspirin’s anti-inflammatory action could potentially counter this, helping explain why CHIP carriers might respond differently.
What This Means for Practice
This study suggests that not all older adults are the same when it comes to aspirin and cancer prevention. For some, aspirin may reduce risk; for others, it may increase it.
The findings are intriguing for the future of personalised prevention strategies, but they don’t yet change clinical recommendations. The US Preventive Services Task Force still concludes that evidence is insufficient to recommend low-dose aspirin for cancer prevention, especially in adults over 60.
As always, aspirin’s risks — most notably bleeding — need to be balanced against its potential benefits in both cardiovascular disease and, possibly, cancer prevention.
Takeaway
Aspirin is unlikely to be a universal cancer-prevention tool. But by incorporating factors like CHIP status, smoking history, and BMI, researchers are moving closer to identifying who might truly benefit.
This could mark the beginning of a more tailored approach to prevention in older adults — one where a simple pill may still have a role, but only for the right patients.
Paper: Thi Phuong Thao, L. et al. Low-Dose Aspirin for Individualized Cancer Prevention in Older Adults: A Secondary Analysis of the ASPREE Randomized Clinical Trial 0 JAMA Oncol. Published online September 25, 2025. doi:10.1001/jamaoncol.2025.3593. Access online here.
