Aspirin but not ibuprofen use is associated with reduced risk of prostate cancer: A PLCO Study

Department of Human Health and Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD, USA.
British Journal of Cancer (Impact Factor: 4.84). 06/2012; 107(1):207-14. DOI: 10.1038/bjc.2012.227
Source: PubMed


Although most epidemiological studies suggest that non-steroidal anti-inflammatory drug use is inversely associated with prostate cancer risk, the magnitude and specificity of this association remain unclear.
We examined self-reported aspirin and ibuprofen use in relation to prostate cancer risk among 29 450 men ages 55-74 who were initially screened for prostate cancer from 1993 to 2001 in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Men were followed from their first screening exam until 31 December 2009, during which 3575 cases of prostate cancer were identified.
After adjusting for potential confounders, the hazard ratios (HRs) of prostate cancer associated with <1 and ≥ 1 pill of aspirin daily were 0.98 (95% confidence interval (CI), 0.90-1.07) and 0.92 (95% CI: 0.85-0.99), respectively, compared with never use (P for trend 0.04). The effect of taking at least one aspirin daily was more pronounced when restricting the analyses to men older than age 65 or men who had a history of cardiovascular-related diseases or arthritis (HR (95% CI); 0.87 (0.78-0.97), 0.89 (0.80-0.99), and 0.88 (0.78-1.00), respectively). The data did not support an association between ibuprofen use and prostate cancer risk.
Daily aspirin use, but not ibuprofen use, was associated with lower risk of prostate cancer risk.

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Available from: Jill Koshiol, Jan 27, 2014
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    • "In a study by Veitonmaki et al. [37] in 2013, a dose–effect relationship was found, indicating a significant inverse association (OR = 0.83) only among participants who used aspirin at the dosage of 37 to 1,300 defined daily dose (DDD). The other benefit was shown among those who took more than one aspirin pill per day [23,29,34], a low dose (≤75 mg/daily) [27,32], larger doses (≥325 mg/daily) [26] or more than six tablets/week [20]; nevertheless, other studies found no evidence of a dose–effect [7,10,17,19,33,35] or frequency–effect [14,16,17] relationship. In terms of the duration of aspirin use, we used the available data from eight studies [15,17-20,26,27,32] with durations of more than four years. "
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    ABSTRACT: It has been postulated that non-steroidal anti-inflammatory drugs (NSAIDs) use leads to decreased prostate cancer (PCa) risk. In recent years, NSAIDs' role in PCa development has been extensively studied; however, there is not yet a definitive answer. Moreover, the epidemiological results for NSAIDs' effect on PCa-specific mortality have been inconsistent. Therefore, we performed a meta-analysis to examine the controversy. We performed a literature database search and included all published studies conducted in the general population exposed to any NSAID, extracting an odds ratio (OR) or a hazard ratio (HR) with 95% confidence intervals (95% CIs) that compared the incidence of PCa or PCa-specific mortality with non-exposure. We derived a pooled OR or HR using random or fixed effects models, as appropriate. Subgroup analyses were also performed. Thirty-nine studies (20 case-control and 19 cohort studies) were included in this analysis. Thirty-one studies were available concerning NSAID use and PCa incidence and eight studies on PCa-specific mortality. Compared to non-use, aspirin use was statistically significantly associated with PCa incidence risk, and the association was slightly stronger for advanced PCa than for total PCa (OR = 0.92, 95% CI = 0.87 to 0.97 for total PCa; OR = 0.81, 95% CI = 0.73 to 0.89 for advanced PCa). Aspirin use seems also to be associated with a modest reduction in PCa-specific mortality (HR = 0.86, 95% CI = 0.78 to 0.96 for total PCa; OR = 0.81, 95% CI = 0.71 to 0.92 for advanced PCa). Generally, the pooled effects for any NSAIDs, NA-NSAIDs and cyclooxygenase-2 inhibitors demonstrated no adverse or beneficial effects on PCa development or PCa-specific mortality, but the results were not consistent. The effect estimates did not vary markedly when stratified by study design and study quality but varied by geographic region. Furthermore, long-term aspirin use (>=4 years) was also significantly associated with reduced PCa incidence (OR = 0.88, 95% CI 0.79 to 0.99). The present meta-analysis provides support for the hypothesis that aspirin use is inversely related to PCa incidence and PCa-specific mortality. The effect estimates, varying by geographic region, deserve further investigation.
    BMC Medicine 03/2014; 12(1):55. DOI:10.1186/1741-7015-12-55 · 7.25 Impact Factor
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    • "Chronic inflammation has been proposed as a risk factor for ovarian cancer 3, 4. Aspirin (acetylsalicylate) is one of the most commonly used nonsteroidal anti-inflammatory drugs in the United States 5, and its use has increased significantly over the last 5 years 6. Although the accumulated evidence shows that aspirin use is associated with a reduced risk of prostate 7, 8, breast 9, colorectal 9, 10 and endometrial cancer 11, the relationship between aspirin and ovarian cancer risk remains controversial. Some investigators have found no association 9, 12-14 while others reported an inverse association between the use of aspirin and ovarian cancer 15-17. "
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    ABSTRACT: Objective: Although aspirin has been associated with a reduction of the risk of cancer when used as a nonsteroidal anti-inflammatory drug, its use to reduce the risk of ovarian cancer is controversial. Ovarian cancer cells usually express high levels of cyclooxygenase-1 (COX)-1. Because aspirin is a rather selective inhibitor of COX-1, the ability of aspirin to reduce the risk of ovarian cancer may be dependent on the level of COX-1 expression in those cells. Furthermore, epidermal growth factor receptor (EGFR) is frequently overexpressed in the malignant phenotype of ovarian cancer leading to increased cell proliferation and survival. Here we investigated if aspirin attenuates EGFR-activated ovarian cancer cell growth in a COX-1 dependent manner. Methods: Cell viability assays and Western blot analyses were used to determine the effect of aspirin on EGF-stimulated cell proliferation. Gene silencing and gene expression techniques were employed to knockdown or to express COX-1, respectively. Results: Aspirin inhibited cell viability induced by EGF in a dose dependent manner in COX-1 positive ovarian cancer cells. On the other hand, aspirin had no effect on cell viability in COX-1 negative ovarian cancer cells. In particular, aspirin decreased phosphorylated Akt and Erk activated by EGF. COX-1 silencing in COX-1 positive cells attenuated the inhibitory effect of aspirin on EGF-stimulated cell viability. Furthermore, we developed a COX-1 expressing cell line (SKCOX-1) by stably transfecting COX-1 expression vector into COX-1 negative SKOV-3 cells. SKCOX-1 cells were more responsive to aspirin when compared to cells transfected with empty vector, and decreased EGF-activated Akt and Erk as well as cell viability. Conclusions: Taken together, aspirin inhibits viability of ovarian cancer cells by blocking phosphorylation of Akt and Erk activated by EGF. Thus it may potentiate the therapeutic efficacy of drugs used to treat COX-1 positive ovarian cancer subsets.
    Journal of Cancer 09/2013; 4(8):671-8. DOI:10.7150/jca.7118 · 3.27 Impact Factor
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    • "COX-2 is overexpressed in numerous premalignant and malignant lesions, including colorectal cancer [20]. It has also been shown that inhibition of inflammatory mediators with anti-inflammatory drugs decreases cancer incidence and progression in patients with cancer [21] [22] [23] [24] [25]. "
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    ABSTRACT: There is a strong relationship between metabolism and immunity, which can become deleterious under conditions of metabolic stress. Obesity, considered a chronic inflammatory disease, is one example of this link. Chronic inflammation is increasingly being recognized as an etiology in several cancers, particularly those of epithelial origin, and therefore a potential link between obesity and cancer. In this review, the connection between the different factors that can lead to the chronic inflammatory state in the obese individual, as well as their effect in tumorigenesis, is addressed. Furthermore, the association between obesity, inflammation, and esophageal, liver, colon, postmenopausal breast, and endometrial cancers is discussed.
    05/2013; 2013(2):697521. DOI:10.1155/2013/697521
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