Tobacco and the risk of pancreatic cancer : a review and meta-analysis

Background/Aim: Smoking is a recognized risk factor for pancreatic cancer. The aim of this study was to perform a meta-analysis to provide a robust estimate of the strength of the association between smoking and pancreatic cancer, to determine the risk of pipe and cigar smoking, and to estimate the duration of an elevated risk after smoking cessation. Methods: We performed a meta-analysis of 82 published studies containing epidemiologic information about smoking and pancreatic cancer. Information on studies published between 1950 and 2007 was abstracted and prepared for analysis using standard meta-analytic procedures. Results: The overall risk of pancreatic cancer estimated from the combined results for current and former smokers was, respectively, 1.74 (95% CI 1.61-1.87) and 1.2 (95% CI 1.11-1.29). The risk of pancreatic cancer for current and former pipe and/or cigar smokers was respectively 1.47 (95% CI 1.17-1.83) and 1.29 (95% CI 0.68-2.45). For former cigarette smokers, the risk remains elevated for a minimum of 10 years after cessation. Conclusions: Based on estimates from four continents, smoking cigarettes causes a 75% increase in the risk of pancreatic cancer compared to non-smokers, and the risk persists for a minimum of 10 years after smoking cessation. This implies that in a population where the prevalence of smoking is 30%, the population's attributable risk (the proportion of pancreatic cancer explained by smoking) is estimated to be 20%

Cigarette smoking and adenomatous polyps : a meta-analysis

Background & Aims: Through the past 2 decades, a consistent association between cigarette smoking and colorectal adenomatous polyps, recognized precursor lesions of colorectal cancer, has been shown. We performed a meta-analysis to provide a quantitative pooled risk estimate of the association, focusing on the different characteristics of the study populations, study designs, and clinical feature of the polyps. Methods: We performed a comprehensive literature search of studies linking cigarette smoking and adenomas. We used random effects models to evaluate pooled relative risks and performed dose-response, heterogeneity, publication bias, and sensitivity analyses. Results: Forty-two independent observational studies were included in the analysis. The pooled risk estimates for current, former, and ever smokers in comparison with never smokers were 2.14 (95% confidence interval [CI], 1.86-2.46), 1.47 (95% CI, 1.29-1.67), and 1.82 (95% CI, 1.65-2.00), respectively. The association was stronger for high-risk adenomas than for low-risk adenomas. Studies in which all controls underwent full colonoscopy showed a higher risk compared with studies in which some or all controls underwent partial colon examination. Conclusions: This meta-analysis provides strong evidence of the detrimental effect of cigarette smoking on the development of adenomatous polyps. Smoking is important for both formation and aggressiveness of adenomas

ABO blood group and cancer

Background: ABO blood type has been associated with various malignancies, including pancreatic cancer. Our aim was to study this association using data from a hospital-based tumour registry. Methods: From the tumour registry, we retrieved data from 15,359 cancer patients treated during 2000-2003 at the European Institute of Oncology (Milan, Italy), with defined ABO blood type. We performed a case-control analysis, comparing the distribution of ABO blood types of patients with each specific form of cancer against that of patients with other forms of cancer. We also reviewed the literature and performed a meta-analysis on the association between ABO blood group and pancreatic cancer. Results: We observed a significantly lower frequency of blood type O in patients with exocrine pancreatic cancer compared to patients with other forms of cancer (29% versus 44%; P < 0.001; odds ratio (OR), 0.53; 95% confidence intervals (CI), 0.33-0.83). This association was confirmed by the meta-analysis of seven prior studies (summary relative risk, 0.79; 95% CI, 0.70-0.90). No association was found for endocrine pancreatic cancer or for cancer originating in other organs. Conclusions: Our data suggest that the association between ABO blood group and cancer is limited to exocrine pancreas malignancy

Gene-smoking interaction on colorectal adenoma and cancer risk : review and meta-analysis

The etiology of colorectal cancer is complex and multifactorial. Tobacco smoke has been found to be associated both with colorectal adenoma and cancer development. It was hypothesized that tobacco smoking could interact with genetic factors, providing different risk estimates according to different genetic predisposition. We reviewed and summarized by a meta-analytic approach the evidence from the literature on the interaction of smoking with the five most studied gene polymorphisms (GSTM1, GSTT1, mEH3, mEH4, NAT2). We calculated pooled Odds Ratios for each gene-smoking combination by random effects models, and provided a pooled P-value for gene-smoking interaction. Heterogeneity among studies was evaluated by the Q statistic and I2. Overall, 27 case-control studies or nested case-control studies are included in this review: 12 presented data on GSTM1 polymorphism, eight on GSTT1, seven on mEH3, mEH4, and 10 on NAT2. We found a weak suggestion of an antagonistic effect of mEH3 low or medium metabolizer with smoking on colorectal adenoma risk (pooled P-value for the interaction: 0.02): smokers carriers of mEH3 low or medium metabolizer had slightly lower risk (Odds Ratio; 95% Confidence Interval: 1.6; 1.2-2.1) than smokers with mEH3 high metabolizer (1.8; 1.4-2.4). A non-significant positive interaction between GSTT1 null genotype and smoking was suggested for colorectal adenoma risk. None of the other common genetic polymorphisms involved in tobacco carcinogens metabolism seemed to modify the smoking-related risk of colorectal adenoma or cancer. \ua9 2009 Elsevier B.V. All rights reserved

Venous thromboembolic events and organ-specific occult cancers : a review and meta-analysis

Background: Despite a recognized association between venous thromboembolic events (VTE) and cancer, little is known about the strength and the features of this association. We performed a meta-analysis in order to clarify this issue. Methods: We retrieved data from 40 reports published between 1982 and 2007: 12 contained cancer risk estimates for patients with either idiopathic or secondary VTE vs. subjects without VTE and 17 for patients with idiopathic vs. secondary VTE. We also pooled risk estimates from four cohort studies to assess the association between VTE and specific forms of cancer and conducted a proportional incidence study, based on the remaining 28 reports, which did not provide risk estimates. Results: The pooled relative risk (RR) of cancer was 3.2 [95% confidence interval (95% CI) 2.4-4.5] for patients with any form of VTE vs. no VTE, 2.7 (95% CI 1.9-3.9) for patients with idiopathic vs. no VTE and 3.8 (95% CI 2.6-5.4) for patients with idiopathic vs. secondary VTE. In the pooled cohort studies, RRs for VTE vs. no VTE were significantly elevated for cancers of the ovary (RR 7.0), pancreas (RR 6.1), liver (RR 5.6), blood (4.2), brain (RR 3.8), kidney (RR 3.4), lung (3.1), colon (2.9), and esophagus (2.1). In the proportional incidence study, cancers of the pancreas, colon, and blood were significantly more frequently observed than in the general population. Conclusions: Overall we found a 3-fold excess risk of occult cancer in patients with VTE. The risk varies according to tumor site and is highest for cancers of the ovary, pancreas, and liver

Risk factors for gallbladder cancer: a Polish case-control study

A population-based case-control study of gallbladder cancer was conducted in the south-west of Poland, within the frame-work of the SEARCH Programme of the International Agency for Research on Cancer. A total of 73 cases and 186 controls were interviewed using a questionnaire including demographic and socio-economic factors, education, smoking, alcohol, tea and coffee consumption, and past medical history. A validated diet history was used to estimate the daily intake of calories, fats, carbohydrates, proteins, cholesterol, fibres and vitamins C and E. Gallbladder disease was the major determinant of subsequent gallbladder cancer: 41 cases (56%) vs. 15 (8%) controls had a past history of gallbladder disease, corresponding to an odds ratio (OR) of 12.5 (95% confidence interval, 5.8 to 26.6), and the OR was 12.1 for gallbladder problems dating back 20 years or more in the past. There was an inverse relationship with education, the OR being 0.3 (95% CI 0.1 to 1.2) for 13 years of education or more vs. less than 7. Gallbladder cancer risk was positively associated with total calorie intake, with ORs of 1.4, 1.5, 4.1 for the 3 upper quartiles compared with the lowest one (trend, p less than 0.01). Weaker direct associations were observed for proteins, carbohydrates and cholesterol. There was some suggestion of inverse associations with fibre intake, and a more consistent one with vitamins C and E. These results further quantify the role of gallstones, and suggest that total calorie intake and other dietary factors potentially linked with benign gallbladder conditions are involved in the aetiology of gallbladder cancer

Liver cirrhosis mortality in Europe, with special attention to Central and Eastern Europe

Background and Aims: Over the last decades, Europe has experienced dramatic changes in the geographical variation of liver cirrhosis rates. We attempt to provide a comprehensive analysis of patterns and trends in liver cirrhosis mortality in European countries and regions. Methods: Age-standardized (world standard) liver cirrhosis mortality rates per 100,000 person-years at ages 20-64 for 35 separate countries were computed using the World Health Organization Mortality Database. Results: In the analyzed period (1959-2002), a very strong East-to-West gradient in mortality rates was observed. An increase of the burden of mortality due to liver cirrhosis appeared in Eastern Europe in two specific areas: South-eastern Europe and North-eastern Europe. In the first group of countries, liver cirrhosis mortality was 10-20 times higher than in most other European states, levels never before observed in Europe. In the countries of North-eastern Europe (former Soviet Union countries) liver cirrhosis mortality was characterized by dramatic changes (both positive and negative) in specific periods of time. Conclusions: Despite the fact that the etiology of liver cirrhosis is multifactorial, it seems that alcohol drinking is the factor that best explains the observed patterns in frequency of this disease in Europe. Alcohol control policies in Central and Eastern Europe could lead to an appreciable reduction of premature mortality from liver cirrhosis. Copyrigh