Ibuprofen is one of the most widely used medicines in the world, prescribed and purchased daily for the management of pain and inflammation. Yet beyond its familiar role in symptom relief, a growing body of research is prompting renewed interest in whether this common NSAID may also influence cancer risk and progression.

As our understanding of the relationship between chronic inflammation and carcinogenesis deepens, ibuprofen has come under scientific scrutiny – raising important questions about whether modulation of inflammatory pathways could have preventive or adjunctive oncological benefits.

NSAIDs, COX inhibition and cancer biology

The link between non-steroidal anti-inflammatory drugs (NSAIDs) and cancer prevention is not new. As early as the 1980s, clinical observations suggested that sulindac, an older NSAID, reduced the incidence of colorectal cancer in high-risk populations. Since then, extensive research has explored whether NSAIDs may exert protective effects across other malignancies.

NSAIDs act primarily by inhibiting cyclooxygenase (COX) enzymes. COX-1 supports physiological processes including gastric mucosal protection, platelet aggregation and renal function, while COX-2 is inducible and plays a key role in inflammatory signalling.

Ibuprofen, like most non-selective NSAIDs, inhibits both isoforms. While this dual action underpins its clinical effectiveness, it also explains its adverse effect profile – particularly gastrointestinal and renal toxicity.

From an oncological perspective, COX-2 inhibition is of particular interest. COX-2–derived prostaglandins are known to promote angiogenesis, tumour proliferation, immune evasion and resistance to apoptosis. Suppressing this pathway may therefore interrupt multiple hallmarks of cancer.

Endometrial cancer: emerging epidemiological signals

One of the most compelling recent findings relates to endometrial cancer, the most common gynaecological malignancy in postmenopausal women. Obesity – a major modifiable risk factor – drives increased oestrogen production and chronic low-grade inflammation, both of which contribute to endometrial carcinogenesis.

A 2025 analysis from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial examined data from over 42,000 women aged 55–74 followed for 12 years. Women reporting regular ibuprofen use (≥30 tablets per month) had a 25% lower risk of developing endometrial cancer compared with those using fewer than four tablets monthly.

Interestingly, this association was strongest among women with pre-existing cardiovascular disease. Aspirin, despite its anti-inflammatory properties, did not demonstrate the same protective effect in this cohort – highlighting that NSAID-related cancer risk modulation may be drug-specific rather than class-wide.

Broader oncological implications

Observational and mechanistic studies suggest ibuprofen may influence the risk or recurrence of several other malignancies, including colorectal, breast, lung and prostate cancers.

In colorectal cancer, ibuprofen use has been associated with reduced tumour growth and lower recurrence rates in survivors. Experimental data also suggest it may impair cancer cell survival, alter hypoxia-related signalling pathways, and increase sensitivity to chemotherapy.

At a molecular level, ibuprofen appears to modulate transcription factors and signalling pathways implicated in tumour survival and immune evasion, including HIF-1α, NFκB and STAT3. It may also influence chromatin structure, altering gene expression in ways that render cancer cells more vulnerable to treatment.

These findings suggest potential multi-level effects that extend beyond simple inflammation suppression.

Conflicting evidence and clinical complexity

Despite these promising signals, the evidence remains inconsistent – and caution is warranted. Some studies have raised concerns about NSAID use following cancer diagnosis. For example, aspirin use after endometrial cancer diagnosis has been associated with increased mortality in certain patient groups, particularly among prior long-term users. Similar concerns have been observed with other NSAIDs.

Systematic reviews present a mixed picture: while NSAIDs (especially aspirin) may reduce the risk of some cancers, regular use of non-aspirin NSAIDs has been linked to increased risk of others, including renal cancer.

These discrepancies highlight the complexity of immune modulation in cancer and underscore the influence of timing, dosage, cancer type, genetics and comorbidities.

Clinical implications and patient safety

Crucially, these findings do not support the use of ibuprofen or other NSAIDs as a preventive strategy in the general population. Long-term or high-dose NSAID use carries well-established risks, including gastrointestinal bleeding, renal impairment and cardiovascular events. Drug–drug interactions, particularly with anticoagulants and antidepressants, further complicate their use.

For clinicians, the current evidence is best viewed as hypothesis-generating rather than practice-changing.

Looking ahead

The idea that a universal analgesic could play a role in cancer prevention is both intriguing and scientifically plausible. If future trials clarify who might benefit, and at what dose and duration, NSAIDs could potentially form part of a stratified prevention or adjuvant treatment approach in high-risk populations.

For now, the strongest evidence for cancer risk reduction remains lifestyle-based: maintaining a healthy weight, engaging in regular physical activity, and adopting dietary patterns that reduce chronic inflammation.

Everyday medicines may yet yield unexpected therapeutic insights – but until the science is settled, cancer prevention remains rooted in prevention, moderation and informed clinical guidance.

Link to research paper: Ibuprofen: how an everyday drug might offer protection against cancer

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