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 \nEurope PMC Funders Group  \nAuthor Manuscript  \nPharmacol Rev. Author manuscript; available in PMC 2026 June 25.  \nPublished in final edited form as:  \nPharmacol Rev. 2026 January 01; 78(1): 100109. doi:10.1016/j.pharmr.2025.100109 .  \nPlatelet activation, aspirin, and cancer: From basic science to clinical trials  \nCarlo Patrono, MD 1,* , John Burn, MD2 , Paola Patrignani, PhD3 , Ruth E. Langley, MD4  \n1 Department of Cardiovascular and Pulmonary Sciences, Catholic University School of Medicine, Rome, Italy  \n2Translational and Clinical Research Institute, Newcastle University, Centre for Life, Newcastle upon Tyne, United Kingdom.  \n3 Department of Neuroscience, Imaging and Clinical Sciences and Center for Advanced Studies and Technology (CAST),“G. d’Annunzio” University of Chieti-Pescara, Chieti, Italy.  \n4MRC Clinical Trials Unit at UCL, University College London, London, United Kingdom.  \nAbstract  \nThere is extensive evidence that aspirin prevents cancer, but the mechanism of action is uncertain. Once-daily low-dose aspirin (75–100 mg) completely and permanently inactivates the cyclooxygenase (COX) activity of prostaglandin G/H synthase-1 (COX-1) in platelets, suppressing thromboxane (TX)A 2-dependent platelet activation. In this article, we review the mechanistic links between platelet activation, inflammation, cancer development, and progression and summarize recent clinical trial results and associated biomarker studies. We hypothesize that persistently enhanced platelet activation has 2 distinct tumorigenic consequences mediated by the release of TXA2 : (1) at sites of gastrointestinal mucosal lesions, it promotes a local inflammatory response with COX-2 induction and enhanced prostaglandin E2 biosynthesis, contributing to early events in carcinogenesis; (2) it inhibits T-cell immunity to cancer by the activation ofTXA2 receptors in lymphocytes, promoting cancer progression and metastasis dissemination. Supporting these  \nThis work is licensed under a CC BY 4.0 International license.  \n*Address correspondence to: Dr Carlo Patrono, Department of Cardiovascular and Pulmonary Sciences, Catholic University School  \nof Medicine, Largo Francesco Vito, 1, 00168 Rome, [Italy. carlo.patrono@unicatt.it](Italy. carlo.patrono@unicatt.it), [john.burn@ncl.ac.uk](john.burn@ncl.ac.uk) .  \nAssociate Editors: Ali Eid and Martin Michel  \nFinancial support  \nThis work was supported by a Cancer Research UK grant to the SPARC Consortium [Grant PRCNPC-NOV24/1000010] . R.E.L. is also supported by the MRC (Medical Research Council) Programme [Grant MC_UU_ 00004/02] .  \nConflict of interest  \nDuring the past 2 years, Carlo Patrono received personal fees from AbbVie; he also reports past grant support (to the institution) for investigator-initiated research from the Italian Drug Agency (AIFA), Bayer, Cancer Research UK (CRUK), and the European Commission; he chaired the Scientific Advisory Board (SAB) of the International Aspirin Foundation. Ruth E. Langley has received research funding from Cancer Research UK and National Institute for Health and Care Research for the Add-Aspirin trial and donation of aspirin and placebo from Bayer PLC for this study; she was a member of the International Aspirin Foundation SAB. All other authors declare no conflicts of interest. John Burn leads the Cancer Prevention Programme responsible for a series of aspirin prevention trials funded by Cancer Research UK and supported by Bayer Pharma who provided active and placebo aspirin tablets for CAPP1, CAPP2 and CaPP3 and contributed to packaging and distribution costs of the CaPP3 trial.  \nCRediT authorship contribution statement  \nCarlo Patrono: Writing – original draft, Writing – review and editing. John Burn: Writing – original draft, Writing – review and editing. Paola Patrignani: Writing – original draft, Writing – review and editing. Ruth E. Langley: Writing – original draft, Writing – review","cbCaijrrAx44H0fh","https://ap.wps.com/l/cbCaijrrAx44H0fh","pdf",2791197,41,"English","# Abstract\n## Mechanistic rationale\n## Tumorigenic consequences via TXA2\n## Scope of evidence and clinical trial context","[{\"question\":\"How does low-dose aspirin affect platelet activity?\",\"answer\":\"Once daily low-dose aspirin (75–100 mg) completely and permanently inactivates platelet COX-1 activity, suppressing TXA2-dependent platelet activation.\"},{\"question\":\"Why is the mechanism of aspirin’s anti-cancer effect considered uncertain?\",\"answer\":\"Although aspirin prevents cancer, the broader pathophysiological and clinical consequences linking TXA2 suppression to cancer development and metastasis are only partially characterized.\"},{\"question\":\"What two tumorigenic consequences are proposed for persistently enhanced platelet activation?\",\"answer\":\"It may (1) promote local inflammatory responses at gastrointestinal mucosal lesion sites through COX-2 induction and increased PGE2 biosynthesis, and (2) suppress T-cell immunity to cancer by activating TXA2 receptors in lymphocytes, facilitating progression and metastasis dissemination.\"}]","Platelet activation, aspirin, and cancer - From basic science to clinical trials | PDF",1790219866,103]