Competing Risk Analysis of Men Aged 55 to 74 Years at Diagnosis Managed Conservatively for Clinically Localized Prostate Cancer

Aspirin and cancer risk: a quantitative review to 2011

At present, only three risk factors for prostate cancer have been firmly established; these are all nonmodifiable: age, race, and a positive family history of prostate cancer. However, numerous modifiable factors have also been implicated in the development of prostate cancer. In the current review, we summarize the epidemiologic data for age, location, and selected behavioral factors in relation to the onset of prostate cancer. Although the available data are not entirely consistent, possible preventative behavioral factors include increased physical activity, intakes of tomatoes, cruciferous vegetables, and soy. Factors that may enhance prostate cancer risk include frequent consumption of dairy products and, possibly, meat. By comparison, alcohol probably exerts no important influence on prostate cancer development. Similarly, dietary supplements are unlikely to protect against the onset of prostate cancer in healthy men. Several factors, such as smoking and obesity, show a weak association with prostate cancer incidence but a positive relation with prostate cancer mortality. Other factors, such as fish intake, also appear to be unassociated with incident prostate cancer but show an inverse relation with fatal prostate cancer. Such heterogeneity in the relationship between behavioral factors and nonadvanced, advanced, or fatal prostate cancers helps shed light on the carcinogenetic process because it discerns the impact of exposure on early and late stages of prostate cancer development. Inconsistent associations between behavioral factors and prostate cancer risk seen in previous studies may in part be due to uncontrolled detection bias because of current widespread use of prostate-specific antigen testing for prostate cancer, and the possibility that certain behavioral factors are systematically related to the likelihood of undergoing screening examinations. In addition, several genes may modify the study results, but data concerning specific gene-environment interactions are currently sparse. Despite large improvements in our understanding of prostate cancer risk factors in the past two decades, present knowledge does not allow definitive recommendations for specific preventative behavioral interventions.

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Risk factors for the onset of prostatic cancer: age, location, and behavioral correlates.

In this Perspectives article, Orsted and Bojesen provide an overview of the literature relating to an association between BPH and prostate cancer, including data from epidemiological studies, in vitro studies, autopsy studies, and randomized controlled trials. They discuss how the measurement of PSA has affected detection and management of the two conditions, and how PSA screening policy is likely to have influenced study findings. They also consider the pathophysiological mechanisms that might explain the observed association between the two diseases, as well as the possible clinical implications of this association.

The link between benign prostatic hyperplasia and prostate cancer

Epidemiological studies have clarified the potential associations between regular aspirin use and cancers. However, it remains controversial on whether aspirin use decreases the risk of cancers risks. Therefore, we conducted an updated meta-analysis to assess the associations between aspirin use and cancers. The PubMed, Embase, and Web of Science databases were systematically searched up to March 2017 to identify relevant studies. Relative risks (RRs) with 95% confidence intervals (CIs) were used to assess the strength of associations. A total of 218 studies with 309 reports were eligible for this meta-analysis. Aspirin use was associated with a significant decrease in the risk of overall cancer (RR = 0.89, 95% CI: 0.87–0.91), and gastric (RR = 0.75, 95% CI: 0.65–0.86), esophageal (RR = 0.75, 95% CI: 0.62–0.89), colorectal (RR = 0.79, 95% CI: 0.74–0.85), pancreatic (RR = 0.80, 95% CI: 0.68–0.93), ovarian (RR = 0.89, 95% CI: 0.83–0.95), endometrial (RR = 0.92, 95% CI: 0.85–0.99), breast (RR = 0.92, 95% CI: 0.88–0.96), and prostate (RR = 0.94, 95% CI: 0.90–0.99) cancers, as well as small intestine neuroendocrine tumors (RR = 0.17, 95% CI: 0.05–0.58). These findings suggest that aspirin use is associated with a reduced risk of gastric, esophageal, colorectal, pancreatic, ovarian, endometrial, breast, and prostate cancers, and small intestine neuroendocrine tumors.

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Associations between aspirin use and the risk of cancers: a meta-analysis of observational studies

Background 
Despite strong laboratory evidence that non-steroidal anti-inflammatory drugs (NSAIDs) could prevent prostate cancer, epidemiological studies have so far reported conflicting results. Most studies were limited by lack of information on dosage and duration of use of the different classes of NSAIDs.
Methods 
We conducted a nested case-control study using data from Saskatchewan Prescription Drug Plan (SPDP) and Cancer Registry to examine the effects of dose and duration of use of five classes of NSAIDs on prostate cancer risk. Cases (N = 9,007) were men aged ≥40 years diagnosed with prostatic carcinoma between 1985 and 2000, and were matched to four controls on age and duration of SPDP membership. Detailed histories of exposure to prescription NSAIDs and other drugs were obtained from the SPDP.
Results 
Any use of propionates (e.g., ibuprofen, naproxen) was associated with a modest reduction in prostate cancer risk (Odds ratio = 0.90; 95%CI 0.84-0.95), whereas use of other NSAIDs was not. In particular, we did not observe the hypothesized inverse association with aspirin use (1.01; 0.95–1.07). There was no clear evidence of dose-response or duration-response relationships for any of the examined NSAID classes.
Conclusions 
Our findings suggest modest benefits of at least some NSAIDs in reducing prostate cancer risk.

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Use of Non-Steroidal Anti-Inflammatory Drugs and Prostate Cancer Risk: A Population-Based Nested Case-Control Study

The prostate specific antigen (PSA) test became available in Saskatchewan in 1990 as a part of the provincial health plan. The purpose of this population-based study was to describe the changes in case mix and treatment patterns for prostate cancer following its introduction. The Saskatchewan Cancer Registry was used to identify all new cases of prostate cancer for the period 1985–2001. We reviewed over 10,000 charts to collect information on tumor characteristics, diagnostic methods, and first choice of treatment. This information was linked to the demographic and mortality data from the registry. The age-adjusted incidence of prostate cancer was influenced greatly by PSA testing volumes. Overall, the rate increased from 90.3 per 100,000 in 1985 to 151.3 per 100,000 in 2001. The increase was mostly organ-confined moderately differentiated cases. The incidence rate of metastatic disease dropped about 50% but only in the 70–79 and 80+ age groups. In 1985, 34% of cases were diagnosed by needle biopsy and 60.4% by TURP. In 2001, the values were 76.1% and 19.7%, respectively. More men now choose radical therapy as the first course of treatment, 81% during 1997–2001 compared to only 63.2% in the 1985–1989 period. Mortality rates remained stable in all age groups over these years. There have been dramatic changes in the case mix of prostate cancers diagnosed since the introduction of PSA testing in the population and significant changes in clinical management of this disease. Thus far, no changes have occurred in mortality rates in the population.

David Skarsgard

Papers

Use of Non-Steroidal Anti-Inflammatory Drugs and Prostate Cancer Risk: A Population-Based Nested Case-Control Study

Changes in case mix and treatment patterns in prostate cancer in Saskatchewan during the prostate specific antigen testing era