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Aspirin reduces cancer risk

Results would be higher if those studies that included the low-dose aspirin (85 mg) were excluded.  All NSAIDs but aspirin increase very significantly the risk for heart attacks--but for aspirin--by accelerating atherosclerosis (American Heart Association warning) MI increased 50% for daily use of Naproxen after 2 years for the elderly (Advantage Study)--jk.


2005, vol. 13, no4, pp. 559-583 [25 page(s) (article)] (264 ref.)  Oncology reports    ISSN  1021-335X 2005, vol. 13, no4, pp. 559-583 [25 page(s) (article)] (264 ref.)

Titre du document / Document title

Aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs in cancer prevention: A critical review of non-selective COX-2 blockade (Review)

Résumé / Abstract

We comprehensively reviewed the published scientific literature on non-steroidal anti-inflammatory drugs (NSAIDs) and cancer and evaluated results based upon epidemiologic criteria of judgment: consistency of results, strength of association, dose response, molecular specificity, and biological plausibility. Sufficient data from 91 epidemiologic studies were available to examine the dose response of relative risk and level of NSAID intake for ten human malignancies. Dose response curves were fitted by exponential regression. Results showed a significant exponential decline in the risk with increasing intake of NSAIDs (primarily aspirin or ibuprofen) for 7-10 malignancies including the four major types: colon, breast, lung, and prostate cancer. Daily intake of NSAIDs, primarily aspirin, produced risk reductions of 63% for colon, 39% for breast, 36% for lung, and 39% for prostate cancer. Significant risk reductions were also observed for esophageal (73%), stomach (62%), and ovarian cancer (47%). NSAID effects became apparent after five or more years of use and were stronger with longer duration. Observed protective effects were also consistently stronger for gastrointestinal malignancies (esophagus, stomach, and colon). Results for pancreatic, urinary bladder, and renal cancer were inconsistent. Initial epidemiologic studies of malignant melanoma, Hodgkin's disease, and adult leukemia also found that NSAIDs are protective. A few studies suggest that ibuprofen has stronger anticancer effects than aspirin, particularly against breast and lung cancer. Overexpression of cyclooxygenase-2 (COX-2) and increased prostaglandin biosynthesis correlates with carcinogenesis and metastasis at most anatomic sites. Preclinical investigations provide consistent evidence that both selective and non-selective NSAIDs effectively inhibit chemically-induced carcinogenesis of epithelial tumors. This review provides compelling and converging evidence that regular intake of NSAIDs that non-selectively block COX-2 protects against the development of many types of cancer.


41% reduction in cancer risk found on moderate usage.  The 1991 population study which increased greatly the awareness of cancer risk reduction--jk New England Journal of Medicine

Aspirin Use and Reduced Risk of Fatal Colon Cancer

Michael J. Thun, M.D., Mohan M. Namboodiri, B.S., and Clark W. Heath, Jr., M.D.

N Engl J Med 1991; 325:1593-1596 December 5, 1991


Background and Methods.

Experiments in animals and two epidemiologic studies in humans suggest that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) may be protective against colon cancer. We tested this hypothesis in a prospective mortality study of 662,424 adults who provided information in 1982 on the frequency and duration of their aspirin use. Death rates from colon cancer were measured through 1988. The possible influence of other risk factors for colon cancer was examined in multivariate analyses for 598 case patients and 3058 matched control subjects drawn from the cohort.

Full Text of Background and Methods. ...


Death rates from colon cancer decreased with more frequent aspirin use in both men and women. The relative risk among persons who used aspirin 16 or more times per month for at least one year was 0.60 in men (95 percent confidence interval, 0.40 to 0.89) and 0.58 in women (95 percent confidence interval, 0.37 to 0.90). The risk estimates were unaffected when we excluded persons who reported at entry into the study that they had cancer, heart disease, stroke, or another condition that might influence both their aspirin use and their mortality. Adjustment for dietary factors, obesity, physical activity, and family history did not alter the findings significantly. No association was found between the use of acetaminophen and the risk of colon cancer.

Full Text of Results. ...


Regular aspirin use at low doses may reduce the risk of fatal colon cancer. Whether this is due to a direct effect of aspirin, perhaps mediated by the inhibition of prostaglandin synthesis, or to other factors indirectly associated with aspirin use is unclear. (N Engl J Med 1991;325:1593—6.)

Full Text of Conclusion


The population studies use the endpoint cause of death, and in general assume that aspirin has no effect upon the course of  treatment or the progression to metastasis ; however, which it does.  Only a couple of studies address this difference.  One study found that 85% of those who took aspirin regularly continued it when they had cancer--jk.  

Aspirin lowers risk of Hodgkin’s lymphoma 60%

 (acetaminophen increased risk 72%, non-aspirin NSAIDs decreased risk 5%).  Criterion for use was those taking 2 or more aspirin per week for 5 years or longer.  Therefor it is likely that higher dose of aspirin per week would confer a greater reduction of Hodgkin’s lymphoma. 

Aspirin and the Risk of Hodgkin's Lymphoma in a Population-Based Case–Control Study

Journal of the National Cancer Institute·  Oxford Journals, ·  Medicine ·  JNCI J Natl Cancer Inst ·  Volume96, Issue4  ·  Pp. 305-315, 


Background: Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with decreased risk of several malignancies. NSAIDs may prevent cancer development by blocking the cyclooxygenase-catalyzed synthesis of proinflammatory prostaglandins. Aspirin may also protect against Hodgkin's lymphoma by inhibiting transcription factor nuclear factor κB (NF-κB), which is necessary for immune function and the survival of Hodgkin's lymphoma cells. We examined the association between regular analgesic use and the risk of Hodgkin's lymphoma. Methods: A population-based case–control study of 565 case patients with Hodgkin's lymphoma and 679 control subjects was conducted in the metropolitan area of Boston, Massachusetts, and in the state of Connecticut. Participants reported their average use of aspirin, non-aspirin NSAIDs, and acetaminophen over the previous 5 years. Regular analgesic use was defined as consumption of at least two tablets per week on average over the preceding 5 years; non-regular use was defined as consumption of fewer than two tablets per week. Results: The risk of Hodgkin's lymphoma associated with regular aspirin use was statistically significantly lower (odds ratio [OR] = 0.60, 95% confidence interval [CI] = 0.42 to 0.85) than that associated with non-regular aspirin use. The risk was not associated with use of other non-aspirin NSAIDs (OR = 0.97, 95% CI = 0.73 to 1.30). However, the risk associated with regular acetaminophen use was statistically significantly higher (OR = 1.72, 95% CI = 1.29 to 2.31) than that associated with non-regular use. Conclusion: The inverse association between aspirin, but not other NSAIDs, and Hodgkin's lymphoma suggests that NF-κB signaling may play a key role in Hodgkin's lymphoma pathogenesis.





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