Coffee consumption and risk of lung cancer: a meta-analysis.
ABSTRACT Epidemiologic studies have evaluated the potential association between coffee consumption and lung cancer risk. However, results were inconsistent. To clarify the role of coffee in lung cancer, we conducted a meta-analysis on this topic. We searched PubMed and EMBASE databases (from 1966 to January 2009) and the reference lists of retrieved articles. Study-specific risk estimates were pooled using random-effects model. Five prospective studies and 8 case-control studies involving 5347 lung cancer cases and 104,911 non-cases were included in this meta-analysis. The combined results indicated a significant positive association between highest coffee intake and lung cancer [relative risk (RR)=1.27, 95% confidence interval (CI)=1.04-1.54). Furthermore, an increase in coffee consumption of 2 cups/day was associated with a 14% increased risk of developing lung cancer (RR=1.14, 95% CI=1.04-1.26). In stratified analyses, the highest coffee consumption was significantly associated with increased risk of lung cancer in prospective studies, studies conducted in America and Japan, but borderline significantly associated with decreased risk of lung cancer in non-smokers. In addition, decaffeinated coffee drinking was associated with decreased lung cancer risk, although the number of studies on this topic was relative small. In conclusion, results from this meta-analysis indicate that high or an increased consumption of coffee may increase the risk of lung cancer. Because the residual confounding effects of smoking or other factors may still exist, these results should be interpreted with caution.
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ABSTRACT: Tea and coffee are the most commonly consumed beverages in the worldwide. The relationship between tea and coffee consumption on the risk of laryngeal cancer was still unclear. Relevant studies were identified by searching electronic database (Medline and EMBASE) and reviewing the reference lists of relevant articles until Oct. 2013. Observational studies that reported RRs and 95% CIs for the link of tea and coffee consumption on the risk of laryngeal cancer were eligible. A meta-analysis was obtained to combine study-specific RRs with a random-effects model. A total of 2,803 cases and 503,234 controls in 10 independent studies were identified. The overall analysis of all 10 studies, including the case-control and cohort studies, found that tea drinking was not associated with laryngeal carcinoma (RR = 1.03; 95% CI: 0.66-1.61). However, coffee consumption was significantly associated with the laryngeal carcinoma (RR = 1.47; 95% CI: 1.03-2.11). A dose-response relationship between coffee intake and laryngeal carcinoma was detected; however, no evidence of dose-response link between tea consumption and laryngeal carcinoma risk was detected. The results from this meta-analysis of observational studies demonstrate that coffee consumption would increase the laryngeal cancer risk, while tea intake was not associated with risk of laryngeal carcinoma.PLoS ONE 01/2014; 9(12):e112006. · 3.53 Impact Factor
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ABSTRACT: Statistics sits right at the heart of scientific endeavour in respiratory medicine and many other disciplines. In this introductory article, some key epidemiological concepts such as representativeness, random sampling, association and causation, and confounding are reviewed. A brief introduction to basic statistics covering topics such as frequentist methods, confidence intervals, hypothesis testing, P values and Type II error is provided. Subsequent articles in this series will cover some modern statistical methods including regression models, analysis of repeated measures, causal diagrams, propensity scores, multiple imputation, accounting for measurement error, survival analysis, risk prediction, latent class analysis and meta-analysis.Respirology 01/2014; 19(1):9-13. · 2.78 Impact Factor
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ABSTRACT: Caffeine causes a diverse range of pharmacological effects that are time- and concentration-dependent and reversible. The detailed mechanisms of caffeine in tumor suppression via tumor suppressor protein p53 remain unclear. The isoforms of p53 are physiological proteins that are expressed in normal cells and generated via alternative promoters, splicing sites and/or translational initiation sites. In this study, we investigated how caffeine modulated cell cycle arrest and apoptosis via the expression of various alternatively spliced p53 isoforms. Caffeine reduced p53α expression and induced the expression of p53β, which contains an alternatively spliced p53 C-terminus. In HeLa cells, the expression levels of many serine/arginine-rich splicing factors, including serine/arginine-rich splicing factors 2 and 3, were altered by caffeine. Serine/arginine-rich splicing factor 3 was a promising candidate for the serine/arginine-rich splicing factors responsible for the alternative splicing of p53 in response to caffeine treatment. In addition to p53-dependent functions, multiple target genes of serine/arginine-rich splicing factor 3 suggest that caffeine can regulate epithelial-mesenchymal-transition and hypoxic conditions to inhibit the survival of tumor cells. In summary, our data provide a new pathway of caffeine-modulated tumor suppression via the alternative splicing of the target genes of serine/arginine-rich splicing factor 3.The international journal of biochemistry & cell biology 12/2013; · 4.89 Impact Factor