A meta-analysis on alcohol drinking and gastric cancer risk

BackgroundWhether an association between alcohol drinking and gastric cancer risk exists is an open question. In order to provide a definite quantification of the association between alcohol drinking and gastric cancer risk, we conducted a meta-analysis of available data.Patients and methods:We carried out a PubMed search of articles published up to June 2010 and identified 44 case–control and 15 cohort studies, including a total of 34 557 gastric cancer cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates. We carried out a dose–risk analysis using nonlinear random-effects meta-regression models.ResultsCompared with nondrinkers, the pooled relative risk (RR) was 1.07 [95% confidence interval (CI) 1.01–1.13] for alcohol drinkers and 1.20 (95% CI 1.01–1.44) for heavy alcohol drinkers (≥4 drinks per day). The pooled estimates were apparently higher for gastric noncardia (RR for heavy drinkers = 1.17, 95% CI 0.78–1.75) than for gastric cardia (RR = 0.99, 95% CI 0.67–1.47) adenocarcinoma. The dose–risk model estimated a RR of 0.95 (95% CI 0.91–0.99) for 10 g/day and 1.14 (95% CI 1.08–1.21) for 50 g/day.ConclusionsThis meta-analysis provides definite evidence of a lack of association between moderate alcohol drinking and gastric cancer risk. There was, however, a positive association with heavy alcohol drinking.     

A meta-analysis on alcohol drinking and esophageal and gastric cardia adenocarcinoma risk

BackgroundIn order to provide a precise quantification of the association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, we conducted a meta-analysis of available data.Patients and methodsWe identified 20 case–control and 4 cohort studies, including a total of 5500 cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates, and we carried out a dose–risk analysis using nonlinear random-effects meta-regression models.ResultsThe relative risk (RR) for drinkers versus nondrinkers was 0.96 [95% confidence interval (CI) 0.85–1.09] overall, 0.87 (95% CI 0.74–1.01) for esophageal adenocarcinoma and 0.89 (95% CI 0.76–1.03) for gastric cardia adenocarcinoma. Compared with nondrinkers, the pooled RRs were 0.86 for light (≤1 drink per day), 0.90 for moderate (1 to <4 drinks per day), and 1.16 for heavy (≥4 drinks per day) alcohol drinking. The dose–risk model found a minimum at 25 g/day, and the curve was <1 up to 70 g/day.ConclusionsThis meta-analysis provides definite evidence of an absence of association between alcohol drinking and esophageal and gastric cardia adenocarcinoma risk, even at higher doses of consumption.     

Alcohol drinking and pancreatic cancer risk: a meta‐analysis of the dose‐risk relation

In order to provide a more precise quantification of the association between alcohol consumption and pancreatic cancer risk, we performed a meta‐analysis of relevant dose‐risk results. We conducted a PubMed search of all case‐control (N=21) and cohort (N=11) studies published up to March 2009. We computed summary relative risk (RR) estimates using either fixed‐ or, in the presence of heterogeneity, random‐effects models. The pooled RR was 0.92 (95% confidence interval, 95% CI, 0.86–0.97) for <3 drinks/day and 1.22 (95% CI, 1.12–1.34) for ≥3 drinks/day. The increased risk for heavy drinking was similar in women and men, but apparently stronger in cohort studies (RR=1.29), in studies with high quality index (RR=1.30), and did not appear to be explained by residual confounding by either history of pancreatitis or tobacco smoking. This meta‐analysis provides strong evidence for the absence of a role of moderate drinking in pancreatic carcinogenesis, coupled to an increased risk for heavy alcohol drinking. Given the moderate increase in risk and the low prevalence of heavy drinkers in most populations, alcohol appears to be responsible only for a small fraction of all pancreatic cancers.     

Tobacco smoking,alcohol consumption and pancreatic cancer risk: A case-control study in Italy

In Italy, pancreatic cancer accounts for approximately 5% of cancer-related deaths. Tobacco smoking is the major established risk factor for this cancer, whereas the role of alcohol consumption is open to debate.Between 1991 and 2008, we conducted a hospital-based case-control study on pancreatic cancer in northern Italy. Cases were 326 patients (median age 63 years) with incident pancreatic cancer admitted to major general hospitals. Controls were 652 patients (median age 63 years) with acute non-neoplastic conditions admitted to the same hospital network of cases. Multiple logistic regression was used to estimate the odds ratios (OR) and the corresponding 95% confidence intervals (CI).Pancreatic cancer was associated to current smoking (OR = 1.68; 95% CI: 1.13–2.48), and the risk rose with increasing number of cigarettes/day (OR = 2.04; 95% CI: 1.14–3.66 for ?20 cigarettes/day). No association emerged for former smokers (OR = 0.98; 95% CI: 0.66–1.45). Alcohol consumption was associated to increased pancreatic cancer risk, but ORs were significant only among heavy drinkers (ORs: 2.03 and 3.42 for 21–34 and ?35 drinks/week, respectively). Pancreatic cancer risk was 4.3-fold higher in heavy smokers (?20 cigarettes/day) and heavy drinkers (?21 drinks/week) in comparison with never smokers who drunk <7 drinks/week, which is compatible with an additive effect of these exposures.In conclusion, we found that tobacco smoking and alcohol drinking are two independent risk factors for pancreatic cancer which may be responsible for approximately one third of these cancers in our population.     

Meta-analysis of 16 studies of the association of alcohol with colorectal cancer

Alcohol consumption is an established risk factor for colorectal cancer (CRC). However, while studies have consistently reported elevated risk of CRC among heavy drinkers, associations at moderate levels of alcohol consumption are less clear. We conducted a combined analysis of 16 studies of CRC to examine the shape of the alcohol–CRC association, investigate potential effect modifiers of the association, and examine differential effects of alcohol consumption by cancer anatomic site and stage. We collected information on alcohol consumption for 14,276 CRC cases and 15,802 controls from 5 case-control and 11 nested case-control studies of CRC. We compared adjusted logistic regression models with linear and restricted cubic splines to select a model that best fit the association between alcohol consumption and CRC. Study-specific results were pooled using fixed-effects meta-analysis. Compared to non-/occasional drinking (≤1 g/day), light/moderate drinking (up to 2 drinks/day) was associated with a decreased risk of CRC (odds ratio [OR]: 0.92, 95% confidence interval [CI]: 0.88–0.98, p = 0.005), heavy drinking (2–3 drinks/day) was not significantly associated with CRC risk (OR: 1.11, 95% CI: 0.99–1.24, p = 0.08) and very heavy drinking (more than 3 drinks/day) was associated with a significant increased risk (OR: 1.25, 95% CI: 1.11–1.40, p < 0.001). We observed no evidence of interactions with lifestyle risk factors or of differences by cancer site or stage. These results provide further evidence that there is a J-shaped association between alcohol consumption and CRC risk. This overall pattern was not significantly modified by other CRC risk factors and there was no effect heterogeneity by tumor site or stage.     

Alcohol drinking and colorectal cancer risk: an overall and dose–response meta-analysis of published studies

BackgroundThe International Agency for Research on Cancer (IARC) concluded that alcohol consumption is related to colorectal cancer (CRC). However, several issues remain unresolved, including quantification of the association for light (≤1 drink/day) and moderate (2–3 drinks/day) alcohol drinking, investigation of the dose–response relationship, and potential heterogeneity of effects by sex, colorectal site, and geographical region.MethodsTwenty-seven cohort and 34 case–control studies presenting results for at least three categories of alcohol intake were identified from a PubMed search of articles published before May 2010. The summary relative risks (RRs) were estimated by the random effects model. Second-order fractional polynomials and random effects meta-regression models were used for modeling the dose–risk relation.ResultsThe RRs were 1.21 [95% confidence interval (CI) 1.13–1.28] for moderate and 1.52 (95% CI 1.27–1.81) for heavy (≥4 drinks/day) alcohol drinking. The RR for moderate drinkers, compared with non-/occasional drinkers, was stronger for men (RR = 1.24, 95% CI 1.13–1.37) than for women (RR = 1.08, 95% CI 1.03–1.13; P_{heterogeneity} = 0.02). For heavy drinkers, the association was stronger in Asian studies (RR = 1.81, 95% CI 1.33–2.46; P_{heterogeneity} = 0.04). The dose–risk analysis estimated RRs of 1.07 (95% CI 1.04–1.10), 1.38 (95% CI 1.28–1.50), and 1.82 (95% CI 1.41–2.35) for 10, 50, and 100 g/day of alcohol, respectively.ConclusionsThis meta-analysis provides strong evidence for an association between alcohol drinking of >1 drink/day and colorectal cancer risk.     

A meta-analysis of alcohol consumption and the risk of brain tumours

BackgroundAlcohol is capable of traversing the blood–brain barrier and is thus a possible risk factor for brain cancer. Several epidemiological studies have been published on the issue, a number of those during recent years, with inconsistent findings.Materials and methodsWe performed a systematic literature search in the Medline and EMBASE databases. We found a total of 19 studies providing risk estimates for total alcohol or specific alcoholic beverages. Pooled estimates of the relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects models.ResultsThe pooled RR of brain cancer for alcohol drinkers versus non-drinkers was 0.97 (95% CI 0.82–1.15; based on 12 studies). Moderate (<2 drinks/day) and heavy alcohol drinkers had RRs of 1.01 (95% CI 0.81–1.25) and 1.35 (95% CI 0.85–2.15), respectively. With reference to specific alcoholic beverages, the RRs were 1.01 (95% CI 0.70–1.48) for wine, 0.96 (95% CI 0.82–1.12) for beer, and 1.20 (95% CI 1.01–1.42) for spirit consumption. The RRs for drinkers versus non-drinkers were 0.93 (95% CI 0.81–1.07) for glioma and 0.71 (95% CI 0.45–1.12) for meningioma.ConclusionsAlcohol drinking does not appear to be associated with adult brain cancer, though a potential effect of high doses deserves further study.     

Alcohol intake and invasive breast cancer risk by molecular subtype and race in the Carolina Breast Cancer Study

Purpose

Alcohol is an established breast cancer risk factor, but there is little evidence on whether the association differs between African Americans and whites.

Methods

Invasive breast cancers (n = 1,795; 1,014 white, 781 African American) and age- and race-matched controls (n = 1,558; 844 white, 714 African American) from the Carolina Breast Cancer Study (Phases I–II) were used to estimate odds ratios (ORs) and 95 % confidence interval (CI) for pre-diagnosis drinks per week and breast cancer risk.

Results

African American controls reported lower alcohol intake than white controls across all age groups. Light drinking (0 to ≤2 per week) was more prevalent among African American controls. Moderate-to-heavy drinking was more prevalent in white controls. African Americans who reported drinking >7 drinks per week had an elevated risk compared to light drinkers [adjusted OR, 95% CI 1.62 (1.03–2.54)]. A weaker association was observed among whites [adjusted OR, 95% CI 1.20 (0.87–1.67)]. The association of >7 drinks per week with estrogen receptor-negative [adjusted OR, 95% CI 2.17 (1.25–3.75)] and triple-negative [adjusted OR, 95% CI 2.12 (1.12–4.04)] breast cancers was significant for African American, but not white women. We observed significantly elevated ORs for heavy intake at ages <25 and >50 years of age for African American women only. We found no evidence of statistical interaction between alcohol intake and oral contraceptive use or smoking.

Conclusions

Drinking more than seven alcoholic beverages per week increased invasive breast cancer risk among white and African American women, with significant increases only among African American women. Genetic or environmental factors that differ by race may mediate the alcohol–breast cancer risk association.

     

Family history and subsite of gastric cancer: Data from a case-referent study in Japan

A comparative case-referent study was conducted using data from the Hospital-Based Epidemiologic Research Program at Aichi Cancer Center (HERPACC) (Nagoya, Japan), with the aim of clarifying the effect of family history on gastric cancer by subsite. Our study comprised 995 histologically confirmed gastric cancer cases (180 cardia, 430 middle, 365 antrum and 20 unclassified) and a total of 43,846 non-cancer outpatients at Aichi Cancer Center Hospital between 1988 and 1995. Logistic regression was used to calculate odds ratios (ORs) for family history of gastric cancer and other cancers, adjusted for age, year and season at first hospital visit, habitual smoking, habitual alcohol drinking, regular physical exercise, preference for salty food and raw vegetable intake. In both genders, a positive family history of gastric cancer was associated with a moderate, but statistically significant increase in risk of gastric cancer [OR = 1.51, 95% confidence interval (95% CI) = 1.29–1.76], while no association was observed between the risk of gastric cancer and a family history of other cancers [OR = 0.97, 95% CI = 0.84–1.13]. OR increased for the middle and antrum parts of gastric cancer, but an increment for the cardiac part was observed only in those with a maternal history of gastric cancer. Our results suggest that the risk of gastric cancer in relation to family history varies by subsite and, furthermore, that the subsite-specific risk of gastric cancer is linked to a maternal history of gastric cancer. Int. J. Cancer 76:801–805, 1998.© 1998 Wiley-Liss, Inc.     

Alcohol consumption and pancreatic cancer: a pooled analysis in the International Pancreatic Cancer Case–Control Consortium (PanC4)

BackgroundHeavy alcohol drinking has been related to pancreatic cancer, but the issue is still unsolved.MethodsTo evaluate the role of alcohol consumption in relation to pancreatic cancer, we conducted a pooled analysis of 10 case–control studies (5585 cases and 11 827 controls) participating in the International Pancreatic Cancer Case–Control Consortium. We computed pooled odds ratios (ORs) by estimating study-specific ORs adjusted for selected covariates and pooling them using random effects models.ResultsCompared with abstainers and occasional drinkers (<1 drink per day), we observed no association for light-to-moderate alcohol consumption (≤4 drinks per day) and pancreatic cancer risk; however, associations were above unity for higher consumption levels (OR = 1.6, 95% confidence interval 1.2–2.2 for subjects drinking ≥9 drinks per day). Results did not change substantially when we evaluated associations by tobacco smoking status, or when we excluded participants who reported a history of pancreatitis, or participants whose data were based upon proxy responses. Further, no notable differences in pooled risk estimates emerged across strata of sex, age, race, study type, and study area.ConclusionThis collaborative-pooled analysis provides additional evidence for a positive association between heavy alcohol consumption and the risk of pancreatic cancer.     

Dietary vitamin D and cancers of the oral cavity and esophagus

BackgroundData on the association between vitamin D and upper digestive tract neoplasms are limited.MethodsIn two case–control studies in Italy, we examined the relation between dietary vitamin D intake and squamous cell carcinoma of the esophagus (SCCE; 304 cases) and oral/pharyngeal cancer (804 cases). Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by multiple logistic regression.ResultsAdjusted ORs for SCCE and oral/pharyngeal cancer were 0.58 (95% CI 0.39–0.86) and 0.76 (95% CI 0.60–0.94), respectively, for the highest tertile of vitamin D intake. Using a reference group of those in the highest tertile of vitamin D who were never/former smokers, ORs were 8.7 (95% CI 4.1–18.7) for SCCE and 10.4 (95% CI 6.9–15.5) for oral/pharyngeal cancer among heavy smokers in the lowest vitamin D tertile; similarly, compared with those in the highest tertile of vitamin D who drank <3 alcoholic drinks/day, corresponding ORs were 41.9 (95% CI 13.7–128.6) for SCCE and 8.5 (95% CI 5.7–12.5) for oral/pharyngeal cancer, among heavy alcohol drinkers in the lowest vitamin D tertile.ConclusionWe observed inverse associations between dietary vitamin D intake and risk of SCCE and, perhaps, oral/pharyngeal cancer, which were most pronounced among heavy current smokers and heavy consumers of alcohol.     

Alcohol and liver cancer: a systematic review and meta-analysis of prospective studies

Despite several studies support a positive association between heavy alcohol consumption and liver cancer risk, a consistent dose–risk relationship has not yet been established. We carried out a systematic review and a meta-analysis of the association between alcohol intake and liver cancer occurrence, following the Meta-analysis Of Observational Studies in Epidemiology guidelines. We searched for cohort and nested case–control studies on the general population published before April 2013, using PubMed and EMBASE. Summary meta-analytic relative risks (RRs) were estimated using random-effect models. We included 16 articles (19 cohorts) for a total of 4445 incident cases and 5550 deaths from liver cancer. Compared with non-drinking, the pooled RRs were 0.91 (95% confidence interval, CI, 0.81–1.02) for moderate drinking (<3 drinks per day) and 1.16 (95% CI, 1.01–1.34) for heavy drinking (≥3 drinks per day), with significant heterogeneity among studies. The dose–risk curve suggested a linear relationship with increasing alcohol intake in drinkers, with estimated excess risk of 46% for 50 g of ethanol per day and 66% for 100 g per day. This systematic review suggests a moderate detrimental role of consumption of 3 or more alcoholic drinks per day on liver cancer, and a lack of association with moderate drinking. Our results have to be taken with due caution on account of the possible limitations of the original studies included in the meta-analysis.     

Alcohol drinking and bladder cancer risk: a meta-analysis

BackgroundWe aimed at investigating the risk of bladder cancer at different levels of alcohol consumption by conducting a meta-analysis of epidemiological studies.Patients and methodsIn October 2010, we carried out a systematic literature search in the Medline database, using PubMed. We identified 16 case–control and 3 cohort studies, including a total of 11 219 cases of bladder cancer, satisfying the inclusion criteria for this meta-analysis. Moderate alcohol intake was defined as <3 drinks per day (i.e. <37.5 g of ethanol per day) and heavy intake as ≥3 drinks/day. Pooled estimates of the relative risks (RR) and the corresponding 95% confidence intervals (CI) were calculated using random effects models.ResultsCompared with non-drinkers, the pooled RRs of bladder cancer were 1.00 (95% CI 0.92–1.09) for moderate and 1.02 (95% CI 0.78–1.33) for heavy alcohol drinkers. When we excluded four studies that did not adjust for tobacco smoking, the corresponding estimates were 0.98 (95% CI 0.89–1.07) and 0.97 (95% CI 0.72–1.31).ConclusionsThis meta-analysis of epidemiological studies provides definite evidence on the absence of any material association between alcohol drinking and bladder cancer risk, even at high levels of consumption.     

Fruit and vegetable consumption,Helicobacter pylori antibodies,and gastric cancer risk: A pooled analysis of prospective studies in China,Japan, and Korea

Epidemiological findings on the association between fruit and vegetable consumption and gastric cancer risk remain inconsistent. The present analysis included 810 prospectively ascertained non‐cardia gastric cancer cases and 1,160 matched controls from the Helicobacter pylori Biomarker Cohort Consortium, which collected blood samples, demographic, lifestyle, and dietary data at baseline. Conditional logistic regression adjusting for total energy intake, smoking, and H. pylori status, was applied to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for gastric cancer risk across cohort‐ and sex‐specific quartiles of fruit and vegetable intake. Increasing fruit intake was associated with decreasing risk of non‐cardia gastric cancer (OR = 0.71, 95% CI: 0.52–0.95, p trend = 0.02). Compared to low‐fruit consumers infected with CagA‐positive H. pylori, high‐fruit consumers without evidence of H. pylori antibodies had the lowest odds for gastric cancer incidence (OR = 0.12, 95% CI: 0.06–0.25), whereby the inverse association with high‐fruit consumption was attenuated among individuals infected with CagA‐positive H. pylori (OR = 0.82, 95% CI: 0.66–1.03). To note, the small number of H. pylori negative individuals does influence this finding. We observed a weaker, nondose‐response suggestion of an inverse association of vegetable intake with non‐cardia gastric cancer risk. High fruit intake may play a role in decreasing risk of non‐cardia gastric cancer in Asia.     

Alcohol drinking and all cancer mortality: a meta-analysis

BackgroundEpidemiological studies have suggested an inconsistent relationship between alcohol drinking and risk of all cancer mortality. As far as we know, no meta-analysis has been conducted to explore this issue.Patients and methodsWe carried out a PubMed search to find relevant articles published before April 2012 in English. Categorical and dose–response meta-analyses were conducted to identify the impact of alcohol drinking on all cancer mortality. Potential sources of heterogeneity were detected by meta-regression and stratification analyses. Sensitivity and cumulative meta-analyses were also carried out.ResultsEighteen independent cohort studies met the inclusion criteria. Compared with non/occasional drinkers, the pooled relative risks (RRs) were 0.91 [95% confidence interval (CI) 0.89–0.94] for light, 1.02 (95% CI 0.99–1.06) for moderate, and 1.31 (95% CI 1.23–1.39) for heavy drinkers. Former drinkers presented a higher risk (RR = 1.32, 95% CI 1.15–1.50) than current drinkers (RR = 1.06, 95% CI 0.98–1.16). There was a J-shaped relationship between all cancer mortality and alcohol consumption in males but not in females.ConclusionsThis meta-analysis confirms the health hazards of heavy drinking (≥50 g/day) and benefits of light drinking (≤12.5 g/day). Large-sample, well-designed, prospective epidemiological studies, especially on heavy drinking among women, should be developed in future.     

Effects of dietary factors and the NAT2 acetylator status on gastric cancer in Koreans

Environmental dietary carcinogens and genetic polymorphisms in metabolic enzymes have been reported to be the risk factors for gastric cancer. This study was undertaken to investigate the effects of the diet, the N‐acetyltransferase (NAT) 2 acetylation status and their interaction on gastric cancer risk. The study population consisted of 471 gastric cancer patients and 471 age‐ and sex‐matched control subjects. NAT2 genotypes were identified using single‐nucleotide primer extension reaction methods. Thirty‐one alleles related to 12 polymorphism sites were assayed in this study. Significantly increased odds ratios were observed in former smokers (OR = 2.39, 95% CI = 1.57–3.62), heavy drinkers (OR = 1.28, 95% CI = 1.06–1.55) and individuals who eat well‐done meat (OR = 1.24, 95% CI = 1.09–1.41). The odds ratios (95% CI) for high intake of kimchi, stews and soybean paste were 3.27 (2.44–4.37), 1.96 (1.50–2.58) and 1.63 (1.24–2.14), respectively. The NAT2 genotype alone was not associated with gastric cancer risk. A significant gene–environment interaction was observed between environmental carcinogens and NAT2 genotypes. The odds ratios for kimchi, stews and soybean paste were higher in slow/intermediate acetylators than in rapid acetylators. The odds ratios for slow/intermediate acetylators were 2.28 (95% CI: 1.29–4.04) for light smokers and 3.42 (95% CI: 2.06–5.68) for well‐done meat intake. The NAT2 acetylator genotype may be an important modifier of the effects of environmental factors on gastric cancer risk. © 2009 UICC     

Single nucleotide polymorphisms of ADH1B,ADH1C and ALDH2 genes and esophageal cancer: A population‐based case–control study in China

Alcohol drinking is a major risk factor for esophageal cancer (EC) and the metabolism of ethanol has been suggested to play an important role in esophageal carcinogenesis. Epidemiologic studies, including genomewide association studies (GWAS), have identified single nucleotide polymorphisms (SNPs) in alcohol dehydrogenases (ADHs) and aldehyde dehydrogenases (ALDHs) to be associated with EC. Using a population‐based case–control study with 858 EC cases and 1,081 controls conducted in Jiangsu Province, China, we aimed to provide further information on the association of ADH1B (rs1229984), ADH1C (rs698) and ALDH2 (rs671) polymorphisms with EC in a Chinese population. Results showed that ADH1B (rs1229984) was associated with EC with odds ratios (ORs) of 1.34 [95% confidence interval (CI): 1.08–1.66] for G‐allele carriers compared to A/A homozygotes. No heterogeneity was detected on this association across different strata of alcohol drinking and tobacco smoking. Statistical interaction between ALDH2 (rs671) and alcohol drinking on EC susceptibility in both additive and multiplicative scales was observed. Compared to G/G homozygotes, A‐allele carriers were positively associated with EC among moderate/heavy drinkers (OR = 1.64, 95% CI: 1.12–2.40) and inversely associated with EC among never/light drinks (OR = 0.75, 95% CI: 0.54–1.03). In addition, statistical interaction between ALDH2 and ADH1B polymorphisms on EC susceptibility among never/light drinkers was indicated. We did not observe association of ADH1C polymorphism with EC. In conclusion, our findings indicated that ADH1B (rs1229984) was associated with EC independent of alcohol drinking and tobacco smoking status and alcohol drinking interacted with ALDH2 (rs671) on EC susceptibility in this high‐risk Chinese population.     

Alcohol consumption,variability in alcohol dehydrogenase genes and risk of renal cell carcinoma

Alcohol consumption has been associated inversely with renal cell carcinoma (RCC) risk; however, no study has examined effect modification by germline variation in alcohol‐metabolizing genes. We investigated whether the association between alcohol intake and RCC risk is modulated by germline variants in alcohol dehydrogenase genes in a large case–control study. Data from 652 RCC cases and 1,366 non‐cancer controls were analyzed. Alcohol intake was assessed using a standardized risk factor questionnaire. Three previously genotyped polymorphisms in ADH6 and ADH7 with the TaqMan assay were examined. Odds ratios (ORs) and 95% confidence interval (CI) were calculated using logistic regression, adjusting for covariates. Compared to non‐drinkers, ever consumption of alcohol was associated with lower RCC risk (OR = 0.52, 95% CI = 0.42–0.65). Analysis with cubic spline regression curve showed a “J‐shaped” relationship between alcohol drinks/day and RCC risk, such that there was no added benefit against RCC for consumption of more than two drinks/day. We observed effect modification by variation in rs1154454 (ADH7) (p_interaction = 0.007); a per unit increase in alcohol drink/day was associated with 35% lower RCC risk among non‐minor allele carriers, a 27% lower risk among those who carry one copy of the minor allele, but no association was observed among those with two copies of the minor allele. These findings indicate that alcohol consumption is associated with lower RCC risk. Consuming more than two drinks a day does not confer additional protection against RCC. The association between alcohol intake and RCC risk appears to be modulated by inter‐individual germline variation in alcohol‐metabolizing genes.     

Risk of gastric cancer among patients with gastric intestinal metaplasia

Plenty of studies have assessed the association between intestinal metaplasia (IM) and gastric cancer risk, while the results were inconsistent. We aimed to assess the risk of gastric cancer among patients with IM. Systematic literature searches were conducted in PubMed, Embase and Cochrane databases. Baseline characteristics and outcomes from the included studies were extracted independently by two investigators. Either a fixed‐effects or a random‐effects model was used to composite the pooled OR for gastric cancer risk. Finally, a total of 21 studies, which comprised 402,636 participants and 4,535 gastric cancer patients, were finally included in the current meta‐analysis. Compared with those participants without IM, IM patients were at a higher risk of gastric cancer (pooled OR = 3.58, 95% CI 2.71–4.73). We observed that incomplete IM (pooled OR = 9.48, 95% CI 4.33–20.78) but not complete IM (pooled OR = 1.55, 95% CI 0.91–2.65) was significantly associated with a higher gastric cancer risk. Besides, it appeared that gastric cancer risk was higher among patients with IM in the corpus (pooled OR = 7.39, 95% CI 4.94–11.06) than those with IM in the antrum only (pooled OR = 4.06, 95% CI 2.79–5.91). And the pooled ORs for gastric noncardia cancer and gastric cardia cancer were 4.98 (95% CI 3.12–7.95) and 1.93 (95% CI 1.15–3.24), respectively. In conclusion, patients with IM were at a higher risk of gastric cancer, especially for incomplete IM and IM in the corpus. The current evidence supports the use of IM subtypes in the surveillance of gastric cancer.     

Alcohol and lung cancer risk among never smokers: A pooled analysis from the international lung cancer consortium and the SYNERGY study

It is not clear whether alcohol consumption is associated with lung cancer risk. The relationship is likely confounded by smoking, complicating the interpretation of previous studies. We examined the association of alcohol consumption and lung cancer risk in a large pooled international sample, minimizing potential confounding of tobacco consumption by restricting analyses to never smokers. Our study included 22 case‐control and cohort studies with a total of 2548 never‐smoking lung cancer patients and 9362 never‐smoking controls from North America, Europe and Asia within the International Lung Cancer Consortium (ILCCO) and SYNERGY Consortium. Alcohol consumption was categorized into amounts consumed (grams per day) and also modelled as a continuous variable using restricted cubic splines for potential non‐linearity. Analyses by histologic sub‐type were included. Associations by type of alcohol consumed (wine, beer and liquor) were also investigated. Alcohol consumption was inversely associated with lung cancer risk with evidence most strongly supporting lower risk for light and moderate drinkers relative to non‐drinkers (>0–4.9 g per day: OR = 0.80, 95% CI = 0.70–0.90; 5–9.9 g per day: OR = 0.82, 95% CI = 0.69–0.99; 10–19.9 g per day: OR = 0.79, 95% CI = 0.65–0.96). Inverse associations were found for consumption of wine and liquor, but not beer. The results indicate that alcohol consumption is inversely associated with lung cancer risk, particularly among subjects with low to moderate consumption levels, and among wine and liquor drinkers, but not beer drinkers. Although our results should have no relevant bias from the confounding effect of smoking we cannot preclude that confounding by other factors contributed to the observed associations. Confounding in relation to the non‐drinker reference category may be of particular importance.