Common cancer risk and statins: a population-based case–control study in a Chinese population

Leung, Henry W.C.; Chan, Agnes L. F.; Lo, Daniel; Leung, John; Chen, Hsiao‐Ling

doi:10.1517/14740338.2013.744392

Cited by 44 publications

(47 citation statements)

References 53 publications

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“…Recently conducted couple of populationbased case-control studies clearly indicate that statins uptake can reduce the risk of gastric cancer [35], and our findings provide further scientific evidence that simvastatin has significant potential for the treatment of gastric cancer and its effects can be further enhanced by capecitabine. Finally, a phase III clinical study of capecitabine/CDDP chemotherapy plus a low dose of simvastatin is already in progress in Korea (http://www.clinicaltrials.gov) and may further help to substantiate our preclinical findings as reported here.…”

Section: Discussionsupporting

confidence: 70%

Simvastatin sensitizes human gastric cancer xenograft in nude mice to capecitabine by suppressing nuclear factor-kappa B-regulated gene products

et al. 2013

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Chemoresistance remains a major problem in the treatment of gastric cancer patients. Hence, novel pharmacological agents that can overcome drug resistance are urgently required. Whether simvastatin can sensitize the gastric cancer to the antitumor effects of capecitabine in vitro and in vivo was investigated. The effect of simvastatin on the proliferation of gastric cancer cells was examined by mitochondrial dyeuptake 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method, apoptosis by esterase staining, NF-κB activation by DNA binding assay, and protein expression by western blot analysis. The effect of simvastatin on the tumor growth in xenograft mouse model of human gastric cancer was also examined. Simvastatin suppressed the proliferation of gastric cancer cells, enhanced the apoptotic effects of capecitabine, suppressed the constitutive activation of NF-κB, and abrogated the expression of cyclooxygenase-2 (COX-2), cyclin D1, Bcl-2, survivin, CXC motif receptor 4, and MMP-9 proteins. In a xenograft mouse model, we observed that the administration of simvastatin alone (5 mg/ kg body weight, intraperitoneal thrice/week) significantly suppressed the growth of the tumor and this effect was further potentiated by capecitabine treatment. As compared to the vehicle control, simvastatin also suppressed the expression of NF-κB-regulated gene products such as cyclin D1, COX-2, ICAM-1, MMP-9, survivin, Bcl-xL, and XIAP in tumor tissues. Overall, our results demonstrate that simvastatin can enhance the effects of capecitabine through suppression of NF-κB-regulated markers of proliferation, invasion, angiogenesis, and metastasis.

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Section: Discussionsupporting

confidence: 70%

Simvastatin sensitizes human gastric cancer xenograft in nude mice to capecitabine by suppressing nuclear factor-kappa B-regulated gene products

et al. 2013

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“…Statins are medication widely used to reduce cholesterol levels and decrease the incidence of cardiovascular and cerebrovascular disease [39]. In addition, increasing evidence shows that statin use is associated with a reduced risk of PD [27, 28].…”

Section: Discussionmentioning

confidence: 99%

Exploring the Association between Statin Use and the Risk of Parkinson’s Disease: A Meta-Analysis of Observational Studies

et al. 2017

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Background: Parkinson’s disease (PD) is a progressive disorder of the central nervous system. The prevalence of PD varies considerably by age group; it has a higher prevalence in patients aged 60 years and more. Several studies have shown that statin, a cholesterol-lowering medication, reduces the risk of developing PD, but evidence for this is so far inconclusive. The objective of this study is to evaluate the association between statin use and the risk of developing PD. Methods: PubMed, EMBASE, and the bibliographies of articles were searched for studies published between January 1, 1990, and January 1, 2017, which reported on the association between statin use and PD. Articles were included if they (1) were published in English, (2) reported patients treated with statin, and the outcome of interest was PD, (3) provided OR/HR with 95% CI or sufficient information to calculate the 95% CI. All abstracts, full-text articles, and sources were reviewed, with duplicate data excluded. Summary relative risk (RRs) with 95% CI was pooled using a random-effects model. Subgroup and sensitivity analyses were also conducted. Results: We selected 16 out of 529 unique abstracts for full-text review using our selection criteria, and 13 out of these 16 studies, comprising 4,877,059 persons, met all of our inclusion criteria. The overall pooled RR of PD was 0.70 (95% CI 0.58–0.84) with significant heterogeneity between estimates (I² = 93.41%, p = 0.000) for the random-effects model. In subgroup analysis, the greater decreased risk was found in studies from Asia (RR 0.62 95% CI 0.51–0.76), whereas a moderate reduction was observed in studies from North America (RR 0.69 95% CI 0.47–1.00), but less reduction was observed in studies from Europe (RR 0.86 95% CI 0.80–0.92). Also, long-term statin use, simvastatin, and atorvastatin showed a higher rate of reduction with significance heterogeneity. Conclusion: Our results showed that statin use is significantly associated with a lower risk of developing PD. Physicians should consider statin drug therapy, monitor its outcomes, and empower their patients to improve their knowledge, therapeutic outcomes, and quality of life. However, preventive measures and their associated mechanisms must be further assessed and explored.

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“…We excluded 139 papers which did not satisfy the inclusion criteria. Seven case control studies [23][24][25][29][30][31][32] were considered to be eligible for this meta-analysis. One study [29] was excluded because data of gastric cancer could not be isolated.…”

Section: Discussionmentioning

confidence: 99%

“…One study [29] was excluded because data of gastric cancer could not be isolated. Finally, six case control studies [23][24][25][30][31][32] were included in this meta-analysis. Table 1 describes baseline characteristics for all six case control studies included.…”

Section: Discussionmentioning

confidence: 99%

“…[16][17][18] As more and more statins are being used, there has been an increasing interest in the preventive effect of statins in cancer. [19][20][21] A meta-analysis of randomized control trials [22] by Shimoyama suggested that statins had no short-term effect on gastric cancer incidence, meanwhile, a population-based nested case control studies demonstrated that prolonged use of statins was not associated with a reducing risk of gastric cancer, [23] however, several case control studies indicated that statins might reduce the rate of gastric cancer recently, [24,25] the effect of statins on gastric cancer risk is still topical and controversial. Thus, we conducted a meta-analysis to evaluate the association of statin exposure and gastric cancer risk.…”

Section: Introductionmentioning

confidence: 99%

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Effect of statins on gastric cancer incidence: A meta-Analysis of case control studies

Wang

Jin

et al. 2014

J Can Res Ther

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Common cancer risk and statins: a population-based case–control study in a Chinese population

Abstract: Overall, the statins suggested a significant reduced risk of the most common cancers in a large Chinese population, particularly in gastric, liver, and uterine cancers.

Cited by 44 publications

References 53 publications

Simvastatin sensitizes human gastric cancer xenograft in nude mice to capecitabine by suppressing nuclear factor-kappa B-regulated gene products

Simvastatin sensitizes human gastric cancer xenograft in nude mice to capecitabine by suppressing nuclear factor-kappa B-regulated gene products

Exploring the Association between Statin Use and the Risk of Parkinson’s Disease: A Meta-Analysis of Observational Studies

Effect of statins on gastric cancer incidence: A meta-Analysis of case control studies

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