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One of the greatest challenges in Europe at the beginning of the 21st Century is the wide east-west health gap. In 2008, the difference in life expectancy between men in some Western European countries and Russia was 20 years. Whilst trends for life expectancy at birth have improved in many areas around the world, those for Russia, as well as those for some other former Soviet Union countries, have fluctuated greatly and have not shown signs of growth since the middle of the 20th Century. This problem is most acute in Russia and former Soviet Union countries, but is also far from being solved in the states that have made significant progress since 1990 and joined the European Union in the 21st Century. One of the priorities of the Polish presidency of the European Union, which began in July 2011, is the call for a European solidarity for health that could help to close the health gap dividing Europe. [ABSTRACT FROM AUTHOR]

The health transformation that took place after the Second World War in Europe was significantly delayed in the Central and Eastern European (CEE) countries compared to countries of Northern Europe and Great Britain. However, as death rates from cardiovascular disease have begun to fall, cancer has emerged, since the 1990s, as the most common cause of death among young and middle-aged adult women (20-64 years old) in these countries. In the coming decade it seems likely to be the leading cause of death among young and middle-aged adult men. MATERIAL AND METHODS: Data on deaths (1959-2002) in each country have been extracted from the World Health Organisation database. Population data are from the Population Division of the Department of Economic and Social Affairs of the United Nations. Direct standardisation has been undertaken using the World Standard Population. RESULTS: The difference in life expectancy attributable to cancer for the 20-64 years of age group is 0.68 of a year (16% of the total gap) among men and 0.35 of a year (24% of the total) among women. Trends in cancer over time differ significantly by gender, age group and time period in Eastern and Western Europe. The predicted mortality rate in CEE in 2015 equates to 201/100,000 (95% CI 199-204) for men and 106/100,000 (95% CI 104-107) for women. CONCLUSIONS: In CEE countries, deficiency of primary prevention is a main reason of poor health consciousness (consequences of smoking, fatty diet, low physical activity) and late introduction of secondary prevention responses results in worse survival of the cancer patient; however, tertiary prevention is implemented in a similar way as in western Europe. Our analysis indicates that the greatest possibilities, but also the greatest unmet needs, lie in primary and secondary prevention. [ABSTRACT FROM AUTHOR]

Background Peptic ulcer and its treatments have been associated to pancreatic cancer risk, although the evidence is inconsistent. Methods We pooled 10 case–control studies within the Pancreatic Cancer Case–control Consortium (PanC4), including 4717 pancreatic cancer cases and 9374 controls, and estimated summary odds ratios (OR) using multivariable logistic regression models. Results The OR for pancreatic cancer was 1.10 [95% confidence interval (CI) 0.98–1.23] for history of ulcer (OR = 1.08 for gastric and 0.97 for duodenal ulcer). The association was stronger for a diagnosis within 2 years before cancer diagnosis (OR = 2.43 for peptic, 1.75 for gastric, and 1.98 for duodenal ulcer). The OR was 1.53 (95% CI 1.15–2.03) for history of gastrectomy; however, the excess risk was limited to a gastrectomy within 2 years before cancer diagnosis (OR = 6.18, 95% CI 1.82–20.96), while no significant increased risk was observed for longer time since gastrectomy. No associations were observed for pharmacological treatments for ulcer, such as antacids, H2-receptor antagonists, or proton-pump inhibitors. Conclusions This uniquely large collaborative study does not support the hypothesis that peptic ulcer and its treatment materially affect pancreatic cancer risk. The increased risk for short-term history of ulcer and gastrectomy suggests that any such association is due to increased cancer surveillance. [ABSTRACT FROM PUBLISHER]

Background To evaluate the dose–response relationship between cigarette smoking and pancreatic cancer and to examine the effects of temporal variables. Methods We analyzed data from 12 case–control studies within the International Pancreatic Cancer Case–Control Consortium (PanC4), including 6507 pancreatic cases and 12 890 controls. We estimated summary odds ratios (ORs) by pooling study-specific ORs using random-effects models. Results Compared with never smokers, the OR was 1.2 (95% confidence interval [CI] 1.0–1.3) for former smokers and 2.2 (95% CI 1.7–2.8) for current cigarette smokers, with a significant increasing trend in risk with increasing number of cigarettes among current smokers (OR = 3.4 for ≥35 cigarettes per day, P for trend <0.0001). Risk increased in relation to duration of cigarette smoking up to 40 years of smoking (OR = 2.4). No trend in risk was observed for age at starting cigarette smoking, whereas risk decreased with increasing time since cigarette cessation, the OR being 0.98 after 20 years. Conclusions This uniquely large pooled analysis confirms that current cigarette smoking is associated with a twofold increased risk of pancreatic cancer and that the risk increases with the number of cigarettes smoked and duration of smoking. Risk of pancreatic cancer reaches the level of never smokers ∼20 years after quitting. [ABSTRACT FROM PUBLISHER]

Background: Heavy alcohol drinking has been related to pancreatic cancer, but the issue is still unsolved. Methods: To 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. Results: Compared 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. Conclusion: This collaborative-pooled analysis provides additional evidence for a positive association between heavy alcohol consumption and the risk of pancreatic cancer. [ABSTRACT FROM PUBLISHER]

Background: Cigarette smoking is the best-characterized risk factor for pancreatic cancer. However, data are limited for other tobacco smoking products and smokeless tobacco.Materials and methods: We conducted a pooled analysis of cigar and pipe smoking and smokeless tobacco use and risk of pancreatic cancer using data from 11 case–control studies (6056 cases and 11 338 controls) within the International Pancreatic Cancer Case-Control Consortium (PanC4). Pooled odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated by unconditional multiple logistic regression models adjusted for study center and selected covariates.Results: Compared with never tobacco users, the OR for cigar-only smokers was 1.6 (95% CI: 1.2–2.3), i.e. comparable to that of cigarette-only smokers (OR 1.5; 95% CI 1.4–1.6). The OR was 1.1 (95% CI 0.69–1.6) for pipe-only smokers. There was some evidence of increasing risk with increasing amount of cigar smoked per day (OR 1.82 for ≥ 10 grams of tobacco), although not with duration. The OR for ever smokeless tobacco users as compared with never tobacco users was 0.98 (95% CI 0.75–1.3).Conclusion: This collaborative analysis provides evidence that cigar smoking is associated with an excess risk of pancreatic cancer, while no significant association emerged for pipe smoking and smokeless tobacco use. [ABSTRACT FROM AUTHOR]

Abstract: Cervical cancer incidence and mortality in Poland is among the highest in Europe. To investigate infection with different human papillomaviruses (HPV) in Warsaw, Poland, we obtained cervical cell specimens from 834 women aged 18–59 years from the general population, and 88 cervical cancers. DNA of 44 HPV types was detected using a GP5+/6+-based PCR assay. HPV prevalence was 16.6% in the general female population, being highest (24.2%) in women aged 25–34 years, notably among unmarried women (37.3%). HPV prevalence fell to 8.6% at ages 55–59. High-risk HPV prevalence was 11.3%, with HPV16 being the most common type (3.7%). All but one cervical cancer were high-risk HPV-positive, although the importance of HPV16 (73%) was much greater, and multiple infections fewer (1%), than among HPV-positive women in the general female population. In summary, we report a relatively high burden of HPV infection in Warsaw, Poland, where 79% of cervical cancers are theoretically preventable by HPV16/18 vaccines. [Copyright &y& Elsevier]

Purpose: Helicobacter pylori infection is a major known risk factor for gastric cancer. The pathogenesis of H. pylori infection is in part mediated by the immunologic reaction, which tend to polarize to a T helper type 1 cells (Th1) cell-mediated response, characterized by high IFN-γ, TNF-a, and IL-2 production. These Th1 prominent cytokines have been demonstrated to activate macrophages to produce proinflammatory cytokines, increase gastrin release, inhibit acid secretion and promote cell apoptosis and proliferation. We evaluated the association of gastric cancer risk with several genetic variants in Th1 related genes, including TNFα (A308G), IL2 (T330G), and IFNGR2 (Q64R, T58R, and 128C>T) in a Polish population. Methods: We conducted a population-based study of 305 gastric cancer cases and 427 controls in Warsaw, Poland, between 1994 and 1996. Controls were randomly selected and frequency matched to cases by sex and age in 5-year groups. Genomic DNA from peripheral blood lymphocytes was used for genotyping, using TaqMan™ assays. Unconditional logistic regression was used to calculate ORs and 95% CIs, adjusting for sex, age, education, and smoking status. Results: Carriers of the TNFa-308 AA genotype were at increased risk of gastric cancer (OR=2.56, 95% CI 1.6–4.1, p-trend &#60;0.001) relative to GG carriers. Of the three polymorphisms that we examined in IFNGR2, only T128C variants were significantly associated with gastric cancer risk (OR=1.79, 95% CI: 1.15–2.78, p-trend=0.009 for CC carriers relative to TT carriers). No clear association was seen for the IL2 (T330G) variant. Subjects carrying both IFNGR2-128 C allele and TNFa-308 AA genotype had the highest risk when compared to carriers of both IFNGR2-128 T allele and TNFa-308 GG genotype (OR=5.11, 95% CI=2.59–10.0, and p &#60; 0.001). Conclusions: Our results suggest that variants in genes involved in Th1 cell-mediated immunologic response may contribute, at least in part, to the etiology of gastric cancer. [Copyright &y& Elsevier]