Statins and cancer: A systematic review and meta-analysis

Kuoppala, Jaana; Lamminpää, Anne; Pukkala, Eero

doi:10.1016/j.ejca.2008.06.025

Cited by 256 publications

(214 citation statements)

References 65 publications

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“…83 --85 These latter studies, however, have also been criticized for short follow-up times, and lack of consideration for the type of statin as well tumor subtype. 78,86,87 When these variables are accounted for, certain statins do appear to confer some degree of protection against cancer incidence or progression. 75,80,81,88 Most importantly, several prospective clinical trials addressing whether statins decrease cancer incidence are now underway.…”

Section: Mid 1970smentioning

confidence: 99%

Targeting tumor cell metabolism with statins

2012

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The mevalonate pathway is a core biochemical process, crucial for the generation of cholesterol and other key metabolic end products. The rate-limiting enzyme of the mevalonate pathway, hydroxymethylglutaryl coenzyme A reductase (HMGCR), is safely and effectively targeted by the statin family of inhibitors to treat hypercholesterolemia. The anticancer activity of statins has also been widely reported, yet the tumor-selective mechanisms that mediate these antiproliferative effects remain largely unclear. The importance of altered metabolism in the context of tumorigenesis has received renewed attention as metabolic changes entwined with the molecular hallmarks of cancer have been elucidated. Although several metabolic pathways have been linked to cancer progression and etiology, it was only recently that HMGCR and the mevalonate pathway were also shown to have a distinct role in cellular transformation. In this review, we chart the historical progression of statins from cholesterol-lowering blockbusters to anticancer agents with imminent potential, and further discuss an emerging role for HMGCR and the mevalonate pathway in the metabolic reprogramming of cancer.

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Section: Mid 1970smentioning

confidence: 99%

Targeting tumor cell metabolism with statins

2012

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“…Finally, we included 80 papers for this overview of reviews, but in our article we only reviewed 55 etiological SRs/meta-analyses (Fu et al, 1995;Huang et al, 1998;Jacobs et al, 1998;Danesh et al, 1999;Eslick et al, 1999;Jia et al, 2000;Wu et al, 2000;Xue et al, 2001;Huang et al, 2003;Guo et al, 2004;Li et al, 2004;Botelho et al, 2006;Hu et al, 2006;Jakszyn et al, 2006;Liu et al, 2006;MacLean et al, 2006;Nishino et al, 2006;Tian et al, 2006;Xu et al, 2006;An et al, 2007;Kubo et al, 2007;Lunet et al, 2007;Merrill et al, 2007;Bae et al, 2008;Ladeiras-Lopes et al, 2008;Kuoppala et al, 2008;Shimazu et al, 2008;Zhou et al, 2008;Huang et al, 2009;La Torre et al, 2009;Mulholland et al, 2009;Myung et al, 2009;Yang et al, 2009;Zhang et al, 2009;Cavaleiro-Pinto et al, 2010;Gatto et al, 2010;Hussein et al, 2010;Kang et al, 2010;Kim et al, 2010;…”

Section: Search Resultsmentioning

confidence: 99%

Overview of Methodological Quality of Systematic Reviews about Gastric Cancer Risk and Protective Factors

Ying²,

Sun³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background and Objective: A comprehensive overall review of gastric cancer (GC) risk and protective factors is a high priority, so we conducted the present study. Methods: Systematic searches in common medical electronic databases along with reference tracking were conducted to include all kinds of systematic reviews (SRs) about GC risk and protective factors. Two authors independently selected studies, extracted data, and evaluated the methodological qualities and the quality of evidence using R-AMSTAR and GRADE approaches. Results: Betacarotene below 20 mg/day, fruit, vegetables, non-fermented soy-foods, whole-grain, and dairy product were GC protective factors, while beta-carotene 20 mg/day or above, pickled vegetables, fermented soy-foods, processed meat 30g/d or above, or salty foods, exposure to alcohol or smoking, occupational exposure to Pb, overweight and obesity, helicobacter pylori infection were GC risk factors. So we suggested screening and treating H. pylori infection, limiting the amount of food containing risk factors (processed meat consumption, beta-carotene, pickled vegetables, fermented soy-foods, salty foods, alcohol), stopping smoking, avoiding excessive weight gain, avoidance of Pb, and increasing the quantity of food containing protective components (fresh fruit and vegetables, non-fermented soy-foods, whole-grain, dairy products). Conclusions: The conclusions and recommendations of our study were limited by including SRs with poor methodological bases and low quality of evidence, so that more research applying checklists about assessing the methodological qualities and reporting are needed for the future.

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“…The relationship between statin use and cancer incidence has been evaluated in numerous epidemiologic studies. Some reports supported a role in cancer chemoprevention (6,28), and others refuted the hypothesis (29). Recently, Lubet et al (30) suggested that atorvastatin and lovastatin fail to inhibit mammary carcinogenesis of rodents.…”

Section: Discussionmentioning

confidence: 99%

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

Toyoda

Tsukamoto²,

Takasu

et al. 2009

Cancer Prevention Research

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Statins are commonly used lipid-lowering drugs that reduce the risk of cardiovascular morbidity and mortality. Although recent studies have pointed to chemopreventive effects of statins against various cancers, their efficacy for gastric cancer is unclear. Here, we examined the effects of pitavastatin, a lipophilic statin, on Helicobacter pylori (H. pylori)-associated stomach carcinogenesis and gastritis using Mongolian gerbil and mouse models. The animals were allocated to H. pylori + N-methyl-N-nitrosourea administration (gerbils, 52 weeks) or H. pylori infection alone groups (gerbils and mice, 12 weeks). After H. pylori infection, they were fed basal diets containing 0 to 10 ppm of pitavastatin. The incidences of H. pylori-associated gastric adenocarcinomas and degrees of chronic gastritis were not decreased by pitavastatin compared with those of control values. Expression of interleukin-1β and tumor necrosis factor-α mRNAs in the pyloric mucosa was markedly up-regulated in pitavastatin-treated animals. Furthermore, in the H. pyloriinfected groups, serum total cholesterol, triglyceride, and low-density lipoprotein levels were significantly increased by pitavastatin treatment, contrary to expectation. In the short-term study, H. pylori-infected gerbils and mice also showed significant up-regulation of serum triglyceride levels by pitavastatin, whereas total cholesterol was markedly reduced and low-density lipoprotein exhibited a tendency for decrease in noninfected animals. These findings indicate pitavastatin to be ineffective for suppressing gastritis and chemoprevention of gastric carcinogenesis in H. pylori-infected gerbils. Our serologic results also suggest that the H. pylori infection and consequent severe chronic gastritis interfere with the cholesterol-lowering effects of pitavastatin.

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Statins and cancer: A systematic review and meta-analysis

Cited by 256 publications

References 65 publications

Targeting tumor cell metabolism with statins

Targeting tumor cell metabolism with statins

Overview of Methodological Quality of Systematic Reviews about Gastric Cancer Risk and Protective Factors

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

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