A Meta-analysis of Alcohol Drinking and Oral and Pharyngeal Cancers: Results from Subgroup Analyses
ABSTRACT AIMS: To quantify the magnitude of the association between alcohol and oral and pharyngeal cancer (OPC) by sex, smoking habits, type of alcoholic beverage and other factors. METHODS: We combined findings from all case-control and cohort studies published until September 2010 and present in this article the results classified by these factors, using a meta-analytic approach. Summary relative risks (RRs) were obtained using random-effects models; heterogeneity was assessed using the χ(2) test. RESULTS: The association between alcohol and OPC risk was similar in men and women, with similar dose-response relationships. No notable differences were found with respect to geographic area and other factors, both for drinking overall and heavy (≥4 drinks/day) drinking. Among never/non-current smokers, the pooled RRs were 1.32 (95% confidence interval, CI, 1.05-1.67) for drinking, and 2.54 (95% CI, 1.80-3.58) for heavy drinking. The corresponding RRs in smokers were 2.92 (95% CI, 2.31-3.70) and 6.32 (95% CI, 5.05-7.90). The pooled RRs for any drinking irrespective of smoking were 2.12 (95% CI, 1.37-3.29) for wine-, 2.43 (95% CI, 1.92-3.07) for beer- and 2.30 (95% CI, 1.78-2.98) for spirits-only drinking. The corresponding RRs for heavy drinking were 4.92 (95% CI, 2.80-8.65), 4.20 (95% CI, 1.43-12.38) and 5.20 (95% CI, 2.77-9.78). CONCLUSION: The alcohol-related RRs are similar with respect to sex, geographic area and type of alcoholic beverage. The association between alcohol and OPC is stronger in smokers than in non-smokers.
- SourceAvailable from: Prakash S Bisen[Show abstract] [Hide abstract]
ABSTRACT: Cancer is a class of diseases characterized by uncontrolled cell growth. The development of cancer takes place in a multi-step process during which cells acquires a series of mutations that eventually lead to unrestrained cell growth and division, inhibition of cell differentiation, and evasion of cell death. Dysregulation of oncoapoptotic genes, growth factors, receptors and their downstream signaling pathway components represent a central driving force in tumor development. The detailed studies of signal transduction pathways for mechanisms of cell growth and apoptosis have significantly advanced our understanding of human cancers, subsequently leading to more effective treatments. Oral squamous cell carcinoma represents a classic example of multi-stage carcinogenesis. It gradually evolves through transitional precursor lesions from normal epithelium to a full-blown metastatic phenotype. Genetic alterations in many genes encoding crucial proteins, which regulate cell proliferation, differentiation, survival and apoptosis, have been implicated in oral cancer. As like other solid tumors, in oral cancer these genes include the ones coding for cell cycle regulators or oncoproteins (e.g. Ras, Myc, cyclins, CDKs, and CKIs), tumor suppressors (e.g. p53 and pRb), pro-survival proteins (e.g. telomerase, growth factors or their receptors), anti-apoptotic proteins (e.g. Bcl2 family, IAPs, and NF-kB), pro-apoptotic proteins (e.g. Bax and BH-3 family, Fas, TNF-R, and caspases), and the genes encoding key transcription factors or elements for signal transduction leading to cell growth and apoptosis. Here we discuss the current knowledge of oncoapoptotic regulation in human cancers with special reference to oral cancers.Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 04/2013; DOI:10.1016/j.bbcan.2013.04.002 · 7.58 Impact Factor
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ABSTRACT: Studies have indicated hazardous consumption of large quantities of alcohol among adults in Lithuania. We assessed the associations of alcohol consumption at baseline with cancer incidence among men in a population-based cohort study, using Cox models adjusted for smoking, education and body mass index. Attained age was used as a time-scale. During follow-up (1978-2008) 1,698 men developed cancer. A higher amount of alcohol consumption (≥140.1 g/week vs. 0.1-10.0 g/week) was positively associated with increased risk of total cancer [hazard ratio (HR) = 1.36, 95 % confidence interval (95 % CI) 1.11, 1.65], upper aerodigestive tract cancer (HR = 2.79, 95 % CI 1.23, 6.34) and alcohol-related cancers (i.e. oral cavity, pharynx, larynx, oesophagus, colorectal and liver cancer) (HR = 1.88, 95 % CI 1.25, 2.85). Compared to occasional drinkers (a few times/year), drinkers 2-7 times/week showed an increased risk of total (HR = 1.45, 95 % CI 1.16, 1.83), alcohol-related (HR = 1.83 95 % CI 1.14, 2.93) and other cancers (HR = 1.35, 95 % CI 1.04, 1.76). Our results showed no statistically significant associations between quantity of alcohol intake per one occasion and risk of cancer. About 13 % of total, 35 % of upper aerodigestive tract, 22 % of alcohol-related and 10 % of other cancer cases were due to alcohol consumption in this cohort of men.European Journal of Epidemiology 05/2013; 28(5). DOI:10.1007/s10654-013-9814-y · 5.15 Impact Factor
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ABSTRACT: To date, the term oral leukoplakia (OL) should be used to recognize ‘predominantly white plaques of questionable risk, having excluded (other) known diseases or disorders that carry no increased risk of cancer’. In this review, we addressed four controversial topics regarding oral leukoplakias (OLs): (i) Do tobacco and alcohol cause OLs?, (ii) What percentage of OLs transform into oral squamous cell carcinoma (OSCC)?, (iii) Can we distinguish between premalignant and innocent OLs?, and (iv) Is proliferative verrucous leukoplakia (PVL) a specific entity or just a form of multifocal leukoplakia? Results of extensive literature search suggest that (i) no definitive evidence for direct causal relationship between smoked tobacco and alcohol as causative factors of OLs, (ii and iii) the vast majority of OLs follow a benign course and do not progress into a cancer, and no widely accepted and/or validated clinical and/or biological factors can predict malignant transformation, and (iv) the distinction between multifocal/multiple leukoplakias and PVL in their early presentation is impossible; the temporal clinical progression and the high rate of recurrences and development of cancer of PVL are the most reliable features for diagnosis.Oral Diseases 10/2013; 19(7). DOI:10.1111/odi.12065 · 2.40 Impact Factor