Aspirin is a widely available over-the-counter medication that shows substantial effects at promoting survival and reducing risk of many types of cancer, plus reducing inflammation and managing pain due to inflammation.
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Modes of action: platelet activity and the NF-κB pathway
Aspirin reversed or inhibited the activity of platelets promoting colorectal or pancreatic cancer cell proliferation and metastasis.1Mitrugno A, Sylman JL et al. Aspirin therapy reduces the ability of platelets to promote colon and pancreatic cancer cell proliferation: implications for the oncoprotein c-MYC. American Journal of Physiology. Cell Physiology. 2017 Feb 1;312(2):C176-C189; Patrignani P, Patrono C. Aspirin, platelet inhibition and cancer prevention. Platelets. 2018 Dec;29(8):779-785.
Aspirin’s inhibition of cyclooxygenases inhibits tumor growth through modulation of the NF-κB pathway.2Chen J, Stark LA. Aspirin prevention of colorectal cancer: focus on NF-κB signalling and the nucleolus. Biomedicines. 2017 Jul 18;5(3). pii: E43.
Preclinical evidence
Notable preclinical evidence is presented here. Clinical evidence is summarized in How can aspirin help you? What the research says ›
Improving treatment outcomes
- Ovarian cancer: phosphatidylcholine-associated aspirin (aspirin-PC) showed anticancer effects in cells and reduced ovarian cancer growth by 50 percent to 90 percent in animals, with no detectable gastrointestinal toxicity; the effect was enhanced in combination with bevacizumab (Avastin) or B20.3Huang Y, Lichtenberger LM et al. Antitumor and antiangiogenic effects of aspirin-PC in ovarian cancer. Molecular Cancer Therapeutics. 2016 Dec;15(12):2894-2904.
Body terrain (immune function)
- Improved antitumor immune response and tumor eradication with aspirin combined with anti-PD1 monoclonal antibody in preclinical studies4Fong W, To KKW. Drug repurposing to overcome resistance to various therapies for colorectal cancer. Cellular and Molecular Life Sciences. 2019;76(17):3383–3406; Zelenay S, van der Veen AG et al. Cyclooxygenase-dependent tumor growth through evasion of immunity. Cell. 2015 Sep 10;162(6):1257-70.
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References