scholarly journals Bisphosphonate use and gastrointestinal tract cancer risk: Meta-analysis of observational studies

2012 ◽  
Vol 18 (40) ◽  
pp. 5779 ◽  
Author(s):  
Yun Hwan Oh
2018 ◽  
Vol 33 (3) ◽  
pp. 244-253 ◽  
Author(s):  
Mohammad Hossein Sahami-Fard

Background: Recent evidence suggests that -592 A/C polymorphism in the interleukin-10 (IL-10) gene may influence risk of gastrointestinal tract cancer; however, individual studies have provided conflicting and inconclusive results. Therefore, this meta-analysis was conducted to assess the association between IL-10 -592 A/C polymorphism and gastrointestinal tract cancer susceptibility. Methods: EMBASE, PubMed, Web of Science, and China National Knowledge Infrastructure databases were searched for case-control studies published before 1 May 2017. A total of 36 studies involving 8069 cases and 13,089 controls were included in the present meta-analysis according to the inclusion criteria. The random- or fixed-effect model was utilized to calculate pooled odds ratio (OR) with 95% confidence interval (CI), and to survey the association. Results: By and large IL-10 -592 A/C (rs1800872) polymorphism was not associated with gastrointestinal cancer risk in five genetic models (A vs. C: OR 1.00; 95% CI 0.93, 1.08; POR = 0.960; AA vs. CC: OR 0.98; 95% CI 0.85, 1.14; POR = 0.835; CA vs. CC: OR 1.01; 95% CI 0.94, 1.08; POR = 0.776; AA+CA vs. CC: OR 1.03; 95% CI 0.94, 1.12; POR = 0.592; AA vs. CA+CC: OR 0.98; 95% CI 0.87, 1.10; POR = 0.666). Similar results were also achieved after stratification by the Hardy–Weinberg equilibrium, ethnicity, source of controls, and cancer type. Conclusion: The results of this meta-analysis indicated that there is no association between the IL-10 -592 A/C promoter polymorphism and gastrointestinal tract cancer susceptibility.


PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e54081 ◽  
Author(s):  
Yan Liu ◽  
Lin Li ◽  
Haiyan Qi ◽  
Yan Gao ◽  
Sha Liu ◽  
...  

Rheumatology ◽  
2012 ◽  
Vol 52 (1) ◽  
pp. 143-154 ◽  
Author(s):  
M. Bonifazi ◽  
I. Tramacere ◽  
G. Pomponio ◽  
B. Gabrielli ◽  
E. V. Avvedimento ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (58) ◽  
pp. 99013-99023 ◽  
Author(s):  
Peng-Liang Wang ◽  
Fang-Tao Xiao ◽  
Bao-Cheng Gong ◽  
Fu-Nan Liu

2005 ◽  
Vol 23 (34) ◽  
pp. 8606-8612 ◽  
Author(s):  
Stefanos Bonovas ◽  
Kalitsa Filioussi ◽  
Nikolaos Tsavaris ◽  
Nikolaos M. Sitaras

Purpose A growing body of evidence suggests that statins may have chemopreventive potential against breast cancer. Laboratory studies demonstrate that statins induce apoptosis and reduce cell invasiveness in various cell lines, including breast carcinoma cells. However, the clinical relevance of these data remains unclear. The nonconclusive nature of the epidemiologic data prompted us to conduct a detailed meta-analysis of the studies published on the subject in peer-reviewed literature. Patients and Methods A comprehensive search for articles published up until 2005 was performed; reviews of each study were conducted; and data were abstracted. Before meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk (RR) estimates and 95% CIs were calculated using the random and the fixed-effects models. Subgroup and sensitivity analyses were also performed. Results Seven large randomized trials and nine observational studies (five case-control and four cohort studies) contributed to the analysis. We found no evidence of publication bias or heterogeneity among the studies. Statin use did not significantly affect breast cancer risk (fixed effects model: RR = 1.03; 95% CI, 0.93 to 1.14; random effects model: RR = 1.02; 95% CI, 0.89 to 1.18). When the analyses were stratified into subgroups, there was no evidence that study design substantially influenced the estimate of effects. Furthermore, the sensitivity analysis confirmed the stability of our results. Conclusion Our meta-analysis findings do not support a protective effect of statins against breast cancer. However, this conclusion is limited by the relatively short follow-up times of the studies analyzed. Further studies are required to investigate the potential decrease in breast cancer risk among long-term statin users.


Sign in / Sign up

Export Citation Format

Share Document