Non‐steroidal anti‐inflammatory drugs and prostate cancer progression

Norrish, Alan; Jackson, Rod; McRae, C

doi:10.1002/(sici)1097-0215(19980812)77:4<511::aid-ijc6>3.3.co;2-t

Cited by 32 publications

(47 citation statements)

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“…We identified 12 reports (10 manuscripts and two unpublished reports) that met the inclusion criteria (Paganini-Hill et al, 1989;Schreinemachers and Everson, 1994;Neugut et al, 1998;Norrish et al, 1998;Langman et al, 2000;Nelson and Harris, 2000;Habel et al, 2002;Irani et al, 2002;Leitzmann et al, 2002;Menezes et al, 2002;Roberts et al, 2002;Perron et al, 2003). Two other studies were excluded because they evaluated outcomes other than incident prostate cancer: a case -control study that measured the prevalence of prostate cancer in autopsies of analgesics abusers (OR ¼ 0.84; 95% confidence interval (CI): 0.36 -1.98) (Bucher et al, 1999) and a cohort study that measured mortality from male genital cancers (rate ratio ¼ 0.82; 95% CI: 0.56 -1.19) (Thun et al, 1993).…”

Section: Resultsmentioning

confidence: 99%

“…Yet, other studies found no evidence of a dose -effect relationship. (Paganini-Hill et al, 1989;Norrish et al, 1998;Langman et al, 2000). The study that was best equipped to address this issue (Perron et al, 2003), in terms of power and availability of detailed exposure data, reported a stronger inverse association with larger doses of aspirin, but only among participants who used aspirin for X4 years.…”

Section: Resultsmentioning

confidence: 99%

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Prostate cancer and use of nonsteroidal anti-inflammatory drugs: systematic review and meta-analysis

2004

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Animal and laboratory studies suggest that regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce prostate cancer risk. To assess this association, we conducted a systematic review and meta-analysis of observational studies published before January 2003. We derived summary odds ratios (ORs) using both fixed and random effects models and performed subgroup analyses to explore the possible sources of heterogeneity between combined studies. We identified 12 reports (five retrospective and seven prospective studies). Most studies of aspirin use reported inverse associations, but only two were statistically significant. The summary OR for the association between aspirin use and prostate cancer was 0.9 (95% confidence interval: 0.82 -0.99; test of homogeneity P ¼ 0.32), and varied from 1.0 for retrospective studies to 0.85 for prospective studies. Studies that measured exposure to a mixture of NSAIDs were less consistent. These results indicate an inverse association between aspirin use and prostate cancer risk. The current epidemiological evidence and, in particular, the strong and consistent laboratory evidence underline the need for additional epidemiological studies to confirm the direction and magnitude of the association.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Prostate cancer and use of nonsteroidal anti-inflammatory drugs: systematic review and meta-analysis

2004

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“…S everal epidemiological studies have shown that the use of nonsteroidal antiinflammatory drugs (NSAIDs) is associated with a reduced incidence of clinically detectable prostate cancer (1)(2)(3). The side effects of cyclooxygenase (COX) inhibitors preclude the use of these agents in many elderly men (4).…”

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confidence: 99%

The R -enantiomer of the nonsteroidal antiinflammatory drug etodolac binds retinoid X receptor and induces tumor-selective apoptosis

Kolluri

Corr

James

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Prostate cancer is often slowly progressive, and it can be difficult to treat with conventional cytotoxic drugs. Nonsteroidal antiinflammatory drugs inhibit the development of prostate cancer, but the mechanism of chemoprevention is unknown. Here, we show that the R-enantiomer of the nonsteroidal antiinflammatory drug etodolac inhibited tumor development and metastasis in the transgenic mouse adenocarcinoma of the prostate (TRAMP) model, by selective induction of apoptosis in the tumor cells. This proapoptotic effect was associated with loss of the retinoid X receptor (RXR␣) protein in the adenocarcinoma cells, but not in normal prostatic epithelium. R-etodolac specifically bound recombinant RXR␣, inhibited RXR␣ transcriptional activity, and induced its degradation by a ubiquitin and proteasome-dependent pathway. The apoptotic effect of R-etodolac could be controlled by manipulating cellular RXR␣ levels. These results document that pharmacologic antagonism of RXR␣ transactivation is achievable and can have profound inhibitory effects in cancer development.cancer ͉ prostate ͉ R-etodolac ͉ ubiquitin ͉ chemoprevention S everal epidemiological studies have shown that the use of nonsteroidal antiinflammatory drugs (NSAIDs) is associated with a reduced incidence of clinically detectable prostate cancer (1-3). The side effects of cyclooxygenase (COX) inhibitors preclude the use of these agents in many elderly men (4). Thus, there is a major need to determine whether there are chemopreventative, and antimetastatic effects of NSAIDs that can be separated from COX inhibition. Controversy has permeated this field, because many of the COX-independent actions of NSAIDs are measurable only at concentrations that are not safely achievable in vivo, and because the members of this structurally diverse group of drugs are metabolized extensively and can exert different mechanisms of action (5, 6).Various NSAIDs have been demonstrated to induce apoptosis in malignant cells (7-9). Etodolac is a commercially available NSAID containing a racemic mixture, in which the S-enantiomer has COX inhibitory activity, whereas the R-enantiomer does not (10). Unlike all other chiral NSAIDs, the two enantiomers of etodolac are not metabolically interconvertible. Moreover, the R-enantiomer is metabolized much more slowly than the S-enantiomer, and it accumulates to 10-fold higher concentrations than the S-enantiomer in plasma (11). In a recent study, sufficient plasma levels of R-etodolac were achieved after oral gavage in a xenograft prostate cancer model to diminish the growth of the transplanted tumor (12).The in vivo effect of R-etodolac was associated with enhancement of peroxisome proliferator-activated receptor ␥ (PPAR␥) transactivation (12). PPAR␥, as well as other nuclear hormone receptors, forms heterodimers with the retinoid X receptor ␣ (RXR␣) (13,14), which has been implicated in the pathogenesis of prostate cancer (15). The effect of RXR␣ may be due to its induction of apoptosis through its interaction with other proteins (16)(17)(18)...

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“…Twenty observational studies with a total of 25 768 participants were included. [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] Characteristics of these studies are presented in Table 1. One study was published in a conference proceeding in 2002, and published again with a smaller sample size in 2005.…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

“…Menezes et al 21 Nelson and Harris 22 Neugut et al 23 Norrish et al 24 Paganini-Hill et al 25 Perron et al 26 Thirteen studies reported the effect of non-ASA NSAIDs with a pooled OR of 0.92 (95% CI 0.85-1.00).…”

Section: Study or Subgroupmentioning

confidence: 99%

Nonsteroidal anti-inflammatory drugs and prostate cancer: a systematic review of the literature and meta-analysis

Jafari

Etminan

Afshar

2013

CUAJ

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Prostate cancer is the most common visceral cancer in men. Many studies have shown that nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce the risk of prostate cancer. We systematically searched all relevant databases (MEDLINE, EMBASE, The Cochrane Collaboration, CINAHL, Database of Abstracts of Review of Effects and ACP Journal Club) to March 2008. We also explored bibliographies of the articles, pertinent journals and conferences. We selected relevant articles according to predefined inclusion criteria by 2 independent reviewers. We used both fixed and randomeffect models for meta-analysis. We performed subgroup and sensitivity analysis based on predefined variables. From 962 extracted articles, 20 met the inclusion criteria with a total of 25 768 participants. All the studies had an observational design. There was a statistically significant protective effect for NSAIDs on risk of prostate cancer (odds ratio [OR] 0.92, 95% confidence interval [CI] 0.86-0.97). Subgroup analysis did not show any effect of study design or quality score on the results. There was a small but statistically significant protective effect for acetylsalicylic acid (ASA) (OR 0.95, 95% CI 0.91-1.00). Exposure to non-ASA NSAIDs was associated with a slightly reduced likelihood of prostate cancer (OR 0.92, 95% CI 0.85-1.00). With the available data, we were not able to determine an optimum dosage for NSAIDs. We conclude that taking NSAIDs may reduce the risk of prostate cancer. Nevertheless, the effect is small. RésuméLe cancer de la prostate est le cancer viscéral le plus fréquent chez l'homme. Bon nombre d'études ont montré que les antiinflammatoires non stéroïdiens (AINS) pouvaient réduire le risque de cancer de la prostate. Notre objectif était de réaliser une revue systématique et une méta-analyse des articles publiés sur les effets des AINS dans la réduction du risque de cancer de la prostate. On a noté un effet protecteur statistiquement significatif sur le risque de cancer de la prostate avec les AINS (rapport de cotes de 0,92; IC à 95 % de 0,86 à 0,97). L'analyse par sous-groupes n'a révélé aucun effet du plan de l'étude ou du score de qualité sur les résultats. On a noté un effet protecteur léger mais tout de même significatif sur le plan statistique avec l'aspirine (RC 0,95; IC à 95 % de 0,91 à 1,00). L'exposition à des AINS autres que l'aspirine a été associée à une probabilité légèrement moindre de cancer de la prostate (RC 0,92, IC à 95 % de 0,85 à 1,00). Les données disponibles ne nous ont pas permis de déterminer la posologie optimale des AINS. Nous avons observé un effet favorable possible associé à la prise d'AINS dans la réduction du risque de cancer de la prostate, mais cet effet est minime.

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Non‐steroidal anti‐inflammatory drugs and prostate cancer progression

Cited by 32 publications

References 4 publications

Prostate cancer and use of nonsteroidal anti-inflammatory drugs: systematic review and meta-analysis

Prostate cancer and use of nonsteroidal anti-inflammatory drugs: systematic review and meta-analysis

The R -enantiomer of the nonsteroidal antiinflammatory drug etodolac binds retinoid X receptor and induces tumor-selective apoptosis

Nonsteroidal anti-inflammatory drugs and prostate cancer: a systematic review of the literature and meta-analysis

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