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Stomach Cancers (stomach + cancers)
Selected AbstractsBreast cancer and microbial cancer incidence in female populations around the world: A surprising hyperbolic associationINTERNATIONAL JOURNAL OF CANCER, Issue 5 2008Anamaria Savu Abstract Current literature on cancer epidemiology typically discusses etiology of cancer by cancer type. Risks of different cancer types are, however, correlated at population level and may provide etiological clues. We showed previously an unexpected very high positive correlation between breast cancer (BC) and young-adult Hodgkin disease incidence rates. In a population-based case,control study of BC, older ages at the first Epstein,Barr virus exposure, indicated by older ages at onset of infectious mononucleosis, were associated with elevated BC risk. Here we examine BC risk in association with microbial cancer (MC) risk in female populations across the world. MC cancers are cervical, liver and stomach cancers with established causal associations with human papillomaviruses, hepatitis viruses, and helicobacter pylori, respectively. We examined age-adjusted BC and MC incidence rates in 74 female populations around the world with cancer registries. Our analysis suggests that BC and MC rates are inversely associated in a special mathematical form such that the product of BC rate and MC rate is approximately constant across world female populations. A differential equation model with solutions consistent to the observed inverse association was derived. BC and MC rates were modeled as functions of an exposure level to unspecified common factors that influence the 2 rates. In conjunction with previously reported evidence, we submit a hypothesis that BC etiology may have an appreciable link with microbial exposures (and/or immunological responses to them), the lack of which, especially in early life, may elevate BC risk. © 2008 Wiley-Liss, Inc. [source] High salt diets dose-dependently promote gastric chemical carcinogenesis in Helicobacter pylori -infected Mongolian gerbils associated with a shift in mucin production from glandular to surface mucous cellsINTERNATIONAL JOURNAL OF CANCER, Issue 7 2006Sosuke Kato Abstract Intake of salt and salty food is known as a risk factor for gastric carcinogenesis. To examine the dose-dependence and the mechanisms underlying enhancing effects, Mongolian gerbils were treated with N -methyl- N -nitrosourea (MNU), Helicobacter pylori and food containing various concentrations of salt, and were sacrificed after 50 weeks. Among gerbils treated with MNU and H. pylori, the incidences of glandular stomach cancers were 15% in the normal diet group and 33%, 36% and 63% in the 2.5%, 5% and 10% NaCl diet groups, showing dose-dependent increase (p < 0.01). Intermittent intragastric injection of saturated NaCl solution, in contrast, did not promote gastric carcinogenesis. In gerbils infected with H. pylori, a high salt diet was associated with elevation of anti- H. pylori antibody titers, serum gastrin levels and inflammatory cell infiltration in a dose-dependent fashion. Ten percent NaCl diet upregulated the amount of surface mucous cell mucin (p < 0.05), suitable for H. pylori colonization, despite no increment of MUC5AC mRNA, while H. pylori infection itself had an opposing effect, stimulating transcription of MUC6 and increasing the amount of gland mucous cell mucin (GMCM). High salt diet, in turn, decreased the amount of GMCM, which acts against H. pylori infection. In conclusion, the present study demonstrated dose-dependent enhancing effects of salt in gastric chemical carcinogenesis in H. pylori -infected Mongolian gerbils associated with alteration of the mucous microenvironment. Reduction of salt intake could thus be one of the most important chemopreventive methods for human gastric carcinogenesis. © 2006 Wiley-Liss, Inc. [source] Asbestos-related cancers among 28,300 military servicemen in the Royal Norwegian NavyAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 1 2010Leif Aage Strand MSc Abstract Introduction This study focus on the incidence of asbestos-related cancers among 28,300 officers and enlisted servicemen in the Royal Norwegian Navy. Until 1987, asbestos aboard the vessels potentially caused exposure to 11,500 crew members. Methods Standardized incidence ratios (SIR) were calculated for malignant mesothelioma, lung cancer, and laryngeal, pharyngeal, stomach, and colorectal cancers according to service aboard between 1950 and 1987 and in other Navy personnel. Results Increased risk of mesothelioma was seen among engine room crews, with SIRs of 6.23 (95% CI,=,2.51,12.8) and 6.49 (95% CI,=,2.11,15.1) for personnel who served less than 2 years and those with longer service, respectively. Lung cancer was nearly 20% higher than expected among both engine crews and non-engine crews. An excess of colorectal cancer bordering on statistical significance was seen among non-engine crews (SIR,=,1.14; 95% CI,=,0.98,1.32). Land-based personnel and personnel who served aboard after 1987 had lower lung cancer incidence than expected (SIR,=,0.77; 95% CI,=,0.64,0.92). No elevated risk of laryngeal, pharyngeal, or stomach cancers was seen. Conclusion The overall increase (65%) in mesotheliomas among military Navy servicemen was confined to marine engine crews only. The mesothelioma incidence can be taken as an indicator of the presence or absence of asbestos exposure, but it offered no consistent explanation to the variation in incidence of other asbestos-related cancers. Am. J. Ind. Med. 53:64,71, 2010. © 2009 Wiley-Liss, Inc. [source] The concerted action of the Helicobacter pylori cytotoxin VacA and of the v-ATPase proton pump induces swelling of isolated endosomesCELLULAR MICROBIOLOGY, Issue 6 2007Christophe Genisset Summary The vacuolating cytotoxin (VacA) is a major virulence factor of Helicobacter pylori, the bacterium associated to gastroduodenal ulcers and stomach cancers. VacA induces formation of cellular vacuoles that originate from late endosomal compartments. VacA forms an anion-selective channel and its activity has been suggested to increase the osmotic pressure in the lumen of these acidic compartments, driving their swelling to vacuoles. Here, we have tested this proposal on isolated endosomes that allow one to manipulate at will the medium. We have found that VacA enhances the v-ATPase proton pump activity and the acidification of isolated endosomes in a Cl, dependent manner. Other counter-anions such as pyruvate, Br,, I, and SCN, can be transported by VacA with stimulation of the v-ATPase. The VacA action on isolated endosomes is associated with their increase in size. Single amino acid substituted VacA with no channel-forming and vacuolating activity is unable to induce swelling of endosomes. These data provide a direct evidence that the transmembrane VacA channel mediates an influx of anions into endosomes that stimulates the electrogenic v-ATPase proton pump, leading to their osmotic swelling and transformation into vacuoles. [source] | ||||||||||