The relationship between statins and breast cancer prognosis varies by statin type and exposure time: A meta-analysis.

Liu, Binliang; Yi, Zongbi; Guan, Xiuwen; Ma, Fei; Zeng, Yi‐Xin

doi:10.1200/jco.2017.35.15_suppl.e21606

Cited by 24 publications

(32 citation statements)

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“…A systematic review and meta‐analysis reported a summary relative risk associating statin use with breast cancer recurrence of 0.64 (95% CI: (0.53–0.79) . Another meta‐analysis showed that statin use was associated with lower breast cancer‐specific mortality (lipophilic statins) and all‐cause mortality (lipophilic and hydrophilic statins) . A third meta‐analysis of observational studies showed that postdiagnostic statin use was associated with lower cancer‐specific mortality in breast cancer, and prediagnostic statin use was negatively associated with both all‐cause and cancer‐specific mortality .…”

Section: Statins and Breast Cancer Prognosismentioning

confidence: 99%

Statins: a role in breast cancer therapy?

et al. 2018

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Statin drugs have been used for more than two decades to treat hypercholesterolemia and as cardio‐preventive drugs, resulting in a marked decrease in cardiovascular morbidity and mortality worldwide. Statins halt hepatic cholesterol biosynthesis by inhibiting the rate‐limiting enzyme in the mevalonate pathway, hydroxymethylglutaryl‐coenzyme A reductase (HMGCR). The mevalonate pathway regulates a host of biochemical processes in addition to cholesterol production. Attenuation of these pathways is likely responsible for the myriad benefits of statin therapy beyond cholesterol reduction – the so‐called pleiotropic effects of statins. Chief amongst these purported effects is anti‐cancer activity. A considerable body of preclinical, epidemiologic and clinical evidence shows that statins impair proliferation of breast cancer cells and reduce the risk of breast cancer recurrence. Potential mechanisms for this effect have been explored in laboratory models, but remain poorly understood and require further investigation. The number of clinical trials assessing the putative clinical benefit of statins in breast cancer is increasing. Currently, a total of 30 breast cancer/statin trials are listed at the global trial identifier website clinicaltrials.gov. Given the compelling evidence from performed trials in a variety of clinical settings, there have been calls for a clinical trial of statins in the adjuvant breast cancer setting. It would be imperative for such a trial to incorporate tumour biomarkers predictive of statin response in its design and analysis plan. Ongoing translational clinical trials aimed at biomarker discovery will help identify, which breast cancer patients are most likely to benefit from adjuvant statin therapy, and will add valuable clinical knowledge to the field.

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Section: Statins and Breast Cancer Prognosismentioning

confidence: 99%

Statins: a role in breast cancer therapy?

et al. 2018

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“…Recent studies demonstrated that stains usage reduces breast cancer-specific mortality in patients with breast cancer. 33,34 Kotamraju et al 35 reported that statins activate arginase-dependent pathways to cause cell death in breast cancer cells. Induction of oxidative stress, 36 stimulation of inducible nitric oxide synthase (iNOS) 35 or alterations of Bax and Bcl-2 levels 37 has been explored as a possible cause of statins' cytotoxicity in MCF-7 breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Lovastatin‐mediated MCF‐7 cancer cell death involves LKB1‐AMPK‐p38MAPK‐p53‐survivin signalling cascade

Huang

Chyuan

Shiue

et al. 2019

J Cellular Molecular Medi

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There is increasing evidence that statins, which are widely used in lowering serum cholesterol and the incidence of cardiovascular diseases, also exhibits anti-tumour properties. The underlying mechanisms by which statins-induced cancer cell death, however, remain incompletely understood. In this study, we explored the anti-tumour mechanisms of a lipophilic statin, lovastatin, in MCF-7 breast cancer cells. Lovastatin inhibited cell proliferation and induced cell apoptosis. Lovastatin caused p21 elevation while reduced cyclin D1 and survivin levels. Lovastatin also increased p53 phosphorylation, acetylation and its reporter activities. Results from chromatin immunoprecipitation analysis showed that p53 binding to the survivin promoter region was increased, while Sp1 binding to the region was decreased, in MCF-7 cells after lovastatin exposure. These actions were associated with liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (p38MAPK) activation. Lovastatin's enhancing effects on p53 activation, p21 elevation and survivin reduction were significantly reduced in the presence of p38MAPK signalling inhibitor. Furthermore, LKB1-AMPK signalling blockade abrogated lovastatin-induced p38MAPK and p53 phosphorylation. Together these results suggest that lovastatin may activate LKB1-AMPK-p38MAPK-p53-survivin cascade to cause MCF-7 cell death. The present study establishes, at least in part, the signalling cascade by which lovastatin induces breast cancer cell death. K E Y W O R D Sbreast cancer, liver kinase B1, lovastatin, p53, surviving Huang and Chyuan contributed equally to this work. | 1823HUANG et Al.

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“…For inpatients, statin administration was documented in the charts within 24 h. Statins cause both acute and chronic changes in metabolism, inflammatory state, and vascular morphology. Studies have shown that many effects of statins last more than 2 days after discontinuation, however, some acute effects of statins may be mitigated by missing a dose [24]. This may introduce some bias, however, any effect introduced by 'wearing away' of some therapeutic effect of statins should drive the results towards null hypothesis, and therefore it should not affect the conclusions derived from this study.…”

Section: Discussionmentioning

confidence: 94%

Reduced risk of post ERCP pancreatitis in statin users

et al. 2020

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Background: One of the most feared complications of endoscopic retrograde cholangiopancreatography (ERCP), with an incidence of 3.5 to 15%, is post ERCP pancreatitis (PEP). Given the role of statins in the reduction of systemic and pancreatic intraluminal inflammation, we hypothesized that the use of statins may lower the risk of PEP. Methods: A retrospective cohort study of all patients undergoing ERCP at West Virginia University during the years 2016 and 2017 was performed. Possible association of collected variables with PEP was assessed with Univariate tests and multivariable logistic regression analyses. Results: A total of 1162 ERCPs were included. Mean age was 60.12 years (SD: 17.5). 51.3% of the participants were female. Two hundred and sixty-three participants underwent more than one ERCP during the study period. Seven hundred and ninety-nine ERCPs (78.8%) were conducted in participants who were not taking a statin medication at the time of ERCP, while 363 participants were on statin medications at the time of ERCP; 118 and 245 participants were taking high dose statins (atorvastatin 40-80 mg or rosuvastatin 20 mg), and low/medium dose statins (all other statin regimens) at the time of the procedure, respectively. The overall incidence of PEP in the cohort was 7.3%. In the non-statin and statin groups, 9.5 and 3.4% of participants developed PEP, respectively. On univariate analysis, young age, no statin use, history of PEP, and endoscopic sphincterotomy were found to be significantly associated with the development of PEP. In a binary logistic regression model, young age (P = 0.033), history of PEP (P = 0.0001, OR 2.41, 95% CI: 1.05-5.51) and endoscopic sphincterotomy (P = 0.038, OR 2.85, 95% CI: 1.7-4.78) were found to be associated with increased risk of PEP. Statin usage was found to be protective against PEP, (OR 0.35, 95% CI: 0.18-0.69). Conclusion: Chronic statin usage is protective against post ERCP pancreatitis, and our findings suggest a potential role of these drugs as prophylactic agents. Randomized controlled trials are needed to establish any potential clinical application.

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The relationship between statins and breast cancer prognosis varies by statin type and exposure time: A meta-analysis.

Cited by 24 publications

References 0 publications

Statins: a role in breast cancer therapy?

Statins: a role in breast cancer therapy?

Lovastatin‐mediated MCF‐7 cancer cell death involves LKB1‐AMPK‐p38MAPK‐p53‐survivin signalling cascade

Reduced risk of post ERCP pancreatitis in statin users

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