Diagnosis of mesothelioma based on death certificate is subject to misclassification, which may bias the results of epidemiology studies. A high proportion of mesothelioma harbor mutations in the ...BRCA1-associated protein 1 (BAP1) gene.
We searched medical and pathology records and specimens for 127 workers from a textile-asbestos factory in Italy who died during 1963–2013 with a diagnosis of pleural or peritoneal neoplasm or mesothelioma on death certificate, to confirm the diagnosis with immunohistochemistry markers. We calculated the odds ratio of confirmation by selected characteristics and asbestos exposure variables. When sufficient pathology material was available, we analyzed BAP1 protein expression.
The diagnosis of mesothelioma was histologically confirmed for 35 cases (27.6%); 5 cases were classified as non-mesothelioma (3.9%), for 33 cases a mention of mesothelioma was found on record but no sufficient material was available for revision (26.0%); no records were available for 54 cases (death-certificate-only 42.5%). Diagnostic confirmation was not associated with sex, location of the neoplasm, age, or duration of employment; however, there was a significant association with time since first employment (P for linear trend 0.04). An association between duration of employment and time since first employment was observed for confirmed cases but not for death-certificate-only cases. BAP1 protein was lost in 18/35 cases (51.4%), without an association with sex, location, age, indices of asbestos exposure, or survival.
We were able to confirm by immunohistochemistry a small proportion of mesothelioma diagnoses on certificates of deceased asbestos workers, and confirmation correlated with latency of asbestos exposure but not other characteristics. BAP1 protein loss is a frequent event in mesothelioma of asbestos-exposed workers, but does not correlate with exposure.
Background: A high consumption of non-starchy vegetables and fruits likely decreases the risk of gastric cancer, but no specific constituent of plant foods has been consistently identified to explain ...this association.
Patients and methods: We considered several micronutrients and minerals in an Italian case–control study conducted between 1997 and 2007, including 230 patients with incident, histologically confirmed gastric cancer and 547 matched controls, admitted with acute conditions. Micronutrients computation was based on a validated and reproducible food frequency questionnaire, through an Italian food composition database. We estimated odds ratios (ORs) using conditional logistic regression, adjusted for energy intake and selected covariates.
Results: We found decreased ORs for the highest versus lowest quartile of vitamin E (OR = 0.50), alpha-carotene (OR = 0.52) and beta-carotene (OR = 0.42) intake. Gastric cancer was directly associated with sodium, with ORs of 2.22 for the second, 2.56 for the third and 2.46 for the fourth quartile of intake. No significant relation emerged with iron, calcium, potassium, zinc, vitamin C, thiamin, riboflavin, niacin, vitamin B6, folate, vitamin D, retinol, beta-cryptoxanthin, lycopene and lutein plus zeaxanthin.
Conclusions: Our data support a favourable effect on gastric cancer of vitamin E and selected carotenoids and a detrimental effect of sodium even at intermediate levels of intake.
In 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.
We ...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.
The 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.
This 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.
The role of alcohol consumption as an independent risk factor for lung cancer is controversial. Since drinking and smoking are strongly associated, residual confounding by smoking may bias the ...estimation of alcohol consumption and lung cancer risk relation. Therefore, we undertook a meta-analysis to quantitatively assess the association between alcohol and risk of lung cancer in never smokers.
After a literature search in Medline, we included all case–control and cohort studies published up to January 2010 that reported an estimate of the association between alcohol intake and lung cancer risk in never smokers.
We selected 10 articles, including 1913 never smoker lung cancer cases. The random-effects pooled relative risk (RR) for drinkers versus nondrinkers was 1.21 95% confidence interval (CI) 0.95–1.55. The same figure was 1.05 (95% CI 0.89–1.23) after the exclusion of one outlier study. At the dose–response analysis, RR for an increase in alcohol intake of 10 g/day was 1.01 (95% CI 0.92–1.10).
Alcohol consumption was not associated with lung cancer risk in never smokers. Even if the synergistic effect of smoking and alcohol cannot be ruled out, our results suggest that alcohol does not play an independent role in lung cancer etiology.
Folate deficiency leads to DNA damage and inadequate repair, caused by a decreased synthesis of thymidylate and purines. We analyzed the relationship between dietary folate intake and the risk of ...several cancers.
The study is based on a network of case–control studies conducted in Italy and Switzerland in 1991–2009. The odds ratios (ORs) for dietary folate intake were estimated by multiple logistic regression models, adjusted for major identified confounding factors.
For a few cancer sites, we found a significant inverse relation, with ORs for an increment of 100 μg/day of dietary folate of 0.65 for oropharyngeal (1467 cases), 0.58 for esophageal (505 cases), 0.83 for colorectal (2390 cases), 0.72 for pancreatic (326 cases), 0.67 for laryngeal (851 cases) and 0.87 for breast (3034 cases) cancers. The risk estimates were below unity, although not significantly, for cancers of the endometrium (OR = 0.87, 454 cases), ovary (OR = 0.86, 1031 cases), prostate (OR = 0.91, 1468 cases) and kidney (OR = 0.88, 767 cases), and was 1.00 for stomach cancer (230 cases). No material heterogeneity was found in strata of sex, age, smoking and alcohol drinking.
Our data support a real inverse association of dietary folate intake with the risk of several common cancers.
The role of alcohol consumption in relation with renal cell carcinoma is still unclear; a few studies have reported a beneficial effect of moderate levels of alcohol consumption, whereas it remains ...still under debate whether there is a dose–response association.
Twenty observational studies (4 cohort, 1 pooled and 15 case–control) reporting results on at least three levels of alcohol consumption were selected through a combined search with PubMed and EMBASE of articles published before November 2010. Overall relative risks (RRs) and 95%confidence intervals (CIs) were estimated using random-effects models, and both second-order fractional polynomials and random effect meta-regression models were implemented for the study of dose–risk relation.
The estimated RRs were 0.85 (95%CI: 0.80–0.92) for any alcohol drinking, 0.90 (95%CI: 0.83–0.97) for light drinking (0.01–12.49 g/day), 0.79 (95%CI: 0.71–0.88) for moderate drinking (12.5–49.9 g/day) and 0.89 (95%CI: 0.58–1.39) for heavy drinking (≥50 g/day), respectively.
Our meta-analysis supports the hypothesis of a negative effect of moderate alcohol consumption on the risk of renal cell cancer.
Occupational exposure to acrylamide was associated with excess mortality from pancreatic cancer, though in the absence of dose-risk relationship. Few epidemiological studies have examined the ...association between acrylamide from diet and pancreatic cancer risk.
We considered this issue in a combined set of 1975 cases of pancreatic cancer and 4239 controls enrolled in six studies of the Pancreatic Cancer Case–Control Consortium (PanC4). We calculated pooled odds ratios (ORs) and their 95% confidence intervals (CI) by estimating study-specific ORs through multivariate unconditional logistic regression models and pooling the obtained estimates using random-effects models.
Compared with the lowest level of estimated dietary acrylamide intake, the pooled ORs were 0.97 (95% CI, 0.79–1.19) for the second, 0.91 (95% CI, 0.71–1.16) for the third, and 0.92 (95% CI, 0.66–1.28) for the fourth (highest) quartile of intake. For an increase of 10 µg/day of acrylamide intake, the pooled OR was 0.96 (95% CI, 0.87–1.06), with heterogeneity between estimates (I2= 67%). Results were similar across various subgroups, and were confirmed when using a one-stage modelling approach.
This PanC4 pooled-analysis found no association between dietary acrylamide and pancreatic cancer.
Abstract Aims The aim of this consensus paper is to review the available evidence on the association between moderate alcohol use, health and disease and to provide a working document to the ...scientific and health professional communities. Data synthesis In healthy adults and in the elderly, spontaneous consumption of alcoholic beverages within 30 g ethanol/d for men and 15 g/d for women is to be considered acceptable and do not deserve intervention by the primary care physician or the health professional in charge. Patients with increased risk for specific diseases, for example, women with familiar history of breast cancer, or subjects with familiar history of early cardiovascular disease, or cardiovascular patients should discuss with their physician their drinking habits. No abstainer should be advised to drink for health reasons. Alcohol use must be discouraged in specific physiological or personal situations or in selected age classes (children and adolescents, pregnant and lactating women and recovering alcoholics). Moreover, the possible interactions between alcohol and acute or chronic drug use must be discussed with the primary care physician. Conclusions The choice to consume alcohol should be based on individual considerations, taking into account the influence on health and diet, the risk of alcoholism and abuse, the effect on behaviour and other factors that may vary with age and lifestyle. Moderation in drinking and development of an associated lifestyle culture should be fostered.
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