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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacters are a new genus of bacteria, inhabiting the interface between mucosa and lumen of the gut. Microaerophilic, spiral, flagellated and urease positive, they possess features necessary for colonisation of the juxtamucosal mucus environment. Helicobacter pylori is the major pathogenic species. Once attached to the gastric epithelial cells, it incites an immune response characterised histologically by the development of active gastritis and immunologically by the presence of specific IgG. Persistence of infection is ensured by attachment to tissue antigens (eg Lewis B), a vacuolating toxin (VacA) which assists the free passage of urea through epithelial cells, and a cytotoxin (CagA) which is actually injected into the epithelial cells via a Type IV secretion system. Finally, during the typical lifelong chronic infection, two important diseases occur. H. pylori alters gastric physiology to cause acid hypersecretion and peptic ulcer. Secondly, it damages the acid secreting mucosa leading to atrophic gastritis and gastric cancer risk.
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PMID:Helicobacter pylori: 20 years on. 1199 Oct 99

Infection by Helicobacter pylori is recognized as a risk factor for gastric cancer and peptic ulcer disease. Venezuela has regions with different gastric cancer risks; the Andean region has the highest gastric cancer mortality in the country. We performed a cross-sectional study on 357 patients who underwent endoscopy attending 2 private (n = 76) and one public hospital in Caracas, Venezuela (n = 215), and one public hospital in the Andes (n = 66) to determine H. pylori infection (by a rapid biopsy urease test and histology). The proportion of infected patients in Caracas was significantly higher in public hospitals (72%) than in private hospitals (46%; P = 0.00001), and there was no significant variation the Andes and Caracas (P = 0.7001). When analyzing the data from the public hospital in Caracas, we found that the frequency of infected patients was significantly higher during the rain (96%) than during the dry months (70%, P = 0.00000001). Differences in prevalence of infection in symptomatic patients was not related to the risk of gastric cancer but to socioeconomic differences. Rain-dependent factors that may be exacerbating the clinical activity of nonulcer dyspepsia in people infected with H. pylori deserve further study.
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PMID:Short report: socioeconomic and seasonal variations of Helicobacter pylori infection in patients in Venezuela. 1213 67

A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. There was no specific relationship between CagA and VacA, and H. pylori infection. Atrophic gastritis and/or intestinal metaplasia were more frequently found in H. pylori-infected relatives of cancer patients (26.1%) than in H. pylori-infected controls (12.9%). These results strongly support a role for H. pylori infection in familial aggregation of gastric cancer. The prophylactic eradication of H. pylori infection in the offspring or siblings of gastric cancer patients may be clinically beneficial.
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PMID:Role of Helicobacter pylori infection among offspring or siblings of gastric cancer patients. 1221 76

Helicobacter pylori, the main cause of chronic gastritis, plays a central role in the etiology of peptic ulcer disease and gastric cancer. In vitro studies have shown that H. pylori increases gastric epithelial cell turnover, thus increasing the risk for the development of neoplastic clones. The mechanisms by which H. pylori promotes perturbation of cell proliferation are not yet elucidated. To investigate whether products released by H. pylori in culture media interfere with cell cycle progression of human gastric epithelial cells, four cell lines (MKN 28, MKN 7, MKN 74, and AGS) were incubated in the presence of H. pylori broth culture filtrate. Cell cycle analysis showed that a H. pylori-released factor(s) significantly inhibited the G1- to S-phase progression of MKN 28 and MKN 7 cell lines, with a reversible, nonlethal mechanism, independent of the expression of VacA, CagA, and/or urease. The cell cycle inhibition occurred concomitantly with an increase in p27(KIP1) protein levels, a reduction in Rb protein phosphorylation on serine residues 807-811, and a significant decrease in cyclin E-associated cdk2 activity. In contrast, the cell cycle progression of MKN 74 and AGS cell lines was not affected by the H. pylori-released factor(s). In normal human fibroblasts, G1-phase cell accumulation was concomitant with the reduction in Rb protein phosphorylation; that, however, appeared to be dependent on p21(WAF1/CIP1) rather than on p27(KIP1) protein. A preliminary characterization showed that the molecular mass of the partially purified cell cycle inhibitory factor(s) was approximately 40 kDa. These results suggest that H. pylori releases a soluble factor(s) that may affect cell cycle progression of gastric epithelial cells through elevated levels of cdk inhibitor p27(KIP1). This factor(s) might act in vivo on noncolonized distant cells, the most proliferating cells of human gastric mucosa.
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PMID:Helicobacter pylori releases a factor(s) inhibiting cell cycle progression of human gastric cell lines by affecting cyclin E/cdk2 kinase activity and Rb protein phosphorylation through enhanced p27(KIP1) protein expression. 1244 Nov 36

Since Marshall's discovery before 20 years, Helicobacter pylori (H. pylori) infection is reportedly to be associated with a variety of clinical outcomes including peptic ulcer disease and gastric cancer. The first step of the H. pylori colonization might be its adhesion to the surface epithelial cells, which evokes gastric inflammatory events initiated by neutrophil recruitment from the microcirculation. Mongolian gerbil is one of the suitable animal models for H. pylori infection, which exerts gastric ulcer and cancer with its bacterial infection. In H. pylori-colonized gerbils, extensive levels of microvascular leukocyte adhesion and migration into the parenchymal side and significant levels of inflammatory cell infiltration are encountered. Bacterial urease not only neutralizes gastric luminal acid, but also plays as an adhesion factor to the surface epithelium. Recently, such an adhesion to the epithelium is reported to be important for bacterial type IV secretory system, which intermediates Cag A injection into the epithelial cells. Then, multiple chemokine and cytokine networks are activated and mucosal inflammatory lesion formation would be completed. In the long-term colonization of H. pylori, gastric mucosal cell turnover would be modified due to persistent inflammation and then such deregulation of cell turnover might link to the precancerous lesion formation.
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PMID:Gastric mucosal response to Helicobacter pylori. 1252 36

Clinical scientists from eight European countries and China gathered in the ancient Chinese capital of Xi'an on April 26-28, 2001 to discuss collaboration on a modern approach to gastric cancer prevention. Participants at the First Sino-European Workshop on Immunogenetics and Pathogenesis of Gastric Cancer presented their most up-to-date research results on topics ranging from epidemiology and immune mechanisms to Helicobacter pylori and vaccine development. Researchers then formed groups with their Chinese or European counterparts to plan future research endeavors which will benefit Chinese and European populations alike. After 3 years of organization between the Institute of Digestive Diseases of the Fourth Medical University in Xi'an, China and the Laboratory of Immunogenetics, VU University Medical Center in Amsterdam, the first workshop came into being under the joint sponsorship of the Commission of the European Union, National Natural Science Foundation of China and the Institute of Digestive Diseases, Xi'an, China. As gastric cancer is the most prevalent malignant tumor in China, the workshop was of special significance to the Chinese researchers and to the Chinese population in general. During the workshop, presentations on the epidemiology of gastric cancer showed that this disease is in fact common the world over: it is the second most common cancer next to lung cancer and about 1 million new cases were diagnosed in 2000. Three-quarters of the cases of gastric cancer occur in Asia, and approximately 80% of these cases are in China and Japan. Genetic factors and environmental factors such as diet and H. pylori infection play a role in gastric carcinogenesis. As a recognized cause of gastric cancer, H. pylori was the subject of various presentations ranging from immunological studies, molecular analysis of strains and pathogenesis to vaccine development. Specific areas of discussion included bacterial-epithelial interactions in H. pylori infection, epidemiology in China, global distribution of vacA and cagA genotypes, new evidence for host factors, nonsteroidal antiinflammatory drugs and H. pylori as independent risk factor for gastric cancer, new diagnostic techniques for H. pylori using serum levels of pepsinogen I, and autoimmune processes in corpus atrophy. Vaccine development using a variety of strategies against H. pylori was the subject of an entire session of talks. Oral immunization with urease with Escherichia coli heat labile enterotoxin was shown to be safe and immunogenic in humans as a mucosal adjuvant. Results of a study using attenuated Salmonella typhimurium as a vehicle for DNA-mediated immunization in mice were also presented. A final presentation discussed an ongoing trial comparing strain variability in the vacA and cagA gene sequences and disease expression between H. pylori infection in Europe and China. Researchers also discussed the role of IL1 gene family and TNF gene polymorphisms in gastric pathology and various immune mechanisms involved in gastric cancer, such as down-regulation of NF kappa B, IL-1 and IL-1RA, cyclooxygenase signalling, and identification of MGAg antibodies. An interactive discussion followed each presentation and ideas and suggestions were provided. According to specialty, the presenters were then assigned to groups of four or five to make plans for joint research projects. A number of international and Chinese observers were present, including representatives from the European Commission, the World Health Organization and the Chinese National Center for Biotechnology Development, and offered input on the financial feasibility of such projects.
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PMID:The immunogenetics and pathogenesis of gastric cancer. Highlights of the First Sino-European Workshop on the Immunogenetics and Pathogenesis of Gastric Cancer. 1253 77

Polymerase chain reaction assay using ureC gene specific primers for the detection of Helicobacter pylori in gastric biopsy specimens from 116 dyspeptic patients was compared with other routine invasive diagnostic methods (culture, rapid urease test [RUT] and histology). In parallel, gastric biospy specimens from 54 patients and their corresponding Helicobacter pylori isolates were subjected to PCR with cagA targeting primers using standard protocols. Helicobacter pylori were detected in 53%, 43%, 48% and 50% of patients by PCR, RUT, culture and histological examination respectively. Based on histology and culture positive and at least three test positive result, 44 (37%), 46 (39%) and 26 (22%), and 56 (48%), 52 (44%) and 8 (6%) patients were classified as Helicobacter pylori positive, negative and indeterminate respectively. The sensitivity and specificity of PCR assay was the highest-95% and 100% when compared with both culture and histology positive, and at least any three positive results respectively. The result of cagA positivity in 54 gastric biopsy specimens and their corresponding Helicobacter pylori isolates were identical; 18 of 20 (90%) duodenal ulcer patients and 23 of 28 (82%) patients with chronic gastritis and 2 (40%) of 5 patients with portal hypertension and one gastric biopsy specimens from gastric cancer patients were found to be cagA positive. PCR-based method to detect Helicobacter pylori and the virulence gene cag A directly from gastric biopsy specimens appears to be promising and can curtail the lengthy process of culture-based approaches. The procedure proved to be rapid and reliable and could be utilized for diagnostic purposes.
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PMID:UreC PCR based diagnosis of Helicobacter pylori infection and detection of cag A gene in gastric biopsies. 1259 61

Helicobacter pylori (H. pylori) is a spiral shaped bacterium that resides in the stomach mucosa. Isolation of H. pylori from the stomach mucosa changed the erstwhile widely held belief that the stomach contains no bacteria and is actually sterile. Once H. pylori is safely ensconced in the mucus, it is able to neutralize the acid in the stomach by elaborating an enzyme called urease. Urease converts urea, of which there is an abundant supply in the stomach (derived from saliva and the gastric juice), into bicarbonate and ammonia, which are strong bases. These bases form a cloud of acid-neutralizing chemicals in the vicinity of the organisms, protecting them from the acid in the stomach. This urea hydrolysis reaction is utilized for the diagnosis of H. pylori infection in the urea breath test (UBT) and the rapid urease test (RUT). In Japan, both invasive tests, such as bacterial culture, histopathology and RUT, and non-invasive tests such as UBT and serology are conducted for the diagnosis of H. pylori infection. For confirming the results of eradication therapy, UBT is considered to be the most sensitive and specific. In order to treat H. pylori infection, a new one-week triple therapy regimen (lansoprazole or omeprazole + amoxicillin + clarithromycin) has been approved for use in patients with peptic ulcer disease in Japan. As for H. pylori eradication in the case of other diseases in which the bacterium has been implicated (e.g., chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, non-ulcer dyspepsia, chronic urticaria, idiopathic thrombocytopenic purpura (ITP)), further basic and clinical investigation is required.
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PMID:Current consensus on the diagnosis and treatment of H. pylori-associated gastroduodenal disease. 1452 49

H. pylori infects the gastric mucosa and causes many digestive disorders such as peptic ulcer, chronic gastritis and gastric cancer. H. pylori infection relates neither to functional health status, nor to intensity of dyspepsia. There is evidence that in most patients with H. pylori positive functional dyspepsia do not improve with eradication of the organism.This study evaluated the diagnostic accuracy of HpSA by determining the sensitivity and specificity of the stool antigen test in predicting successful eradication during and after anti microbial therapy. The work was conducted on patients who underwent upper gastrointestinal endoscopy at Al-Azhar University hospitals. Fifty patients (34 male & 16 female) with dyspepsia were selected, the exclusion criteria included use of antibiotics and proton pump inhibitors up to one month before the study. All cases were submitted to, full history, general and local examination and upper gastrointestinal endoscopy. Biopsies were taken from the antrum and body of the stomach for rapid urease test and histopathology. Stool samples were taken to detect H. pylori stool antigen. Positive patients received eradication treatment for one month and H. pylori status was re-determined by rapid urease test, histological examination and HpSA test one month later. H. pylori was detected by rapid urease test in 29 (58%) dyspeptic patient by histology in 26(52%) dyspeptic patient, while H. pylori was detected by HpSA immunoassay in 16 (32%) dyspeptic patient. The sensitivity and specificity of HpSA were 57.7% and 95.8% respectively. After successful eradication of H. pylori, reassessment by rapid urease test and histology revealed curative rate of 86.2% and 84.6% respectively, while HpSA immunoassay revealed curative rate 75%. Based on these results, the HpSA immunoassay gave sensitivity (75%) and specificity (100%). The H. pylori stool test represents an accurate and novel non-invasive concept for diagnosis of infection and can be used for daily routine in clinical practice. HpSA is a promising non-invasive test for diagnosis of H. pylori infection but may be hampered by low patient acceptability. So, HpSA is a valuable test in the pre-and post eradication assessment of infection. HpSA can be profitably employed in the primary diagnosis of H. pylori infection. This non invasive test could be very useful in investigating dyspeptic young patients. Also, it could be used profitably in epidemiological studies to determine the prevalence of H. pylori infection in the asymptomatic subjects in different communities.
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PMID:Evaluation of a new enzyme immunoassay for the detection of Helicobacter pylori in stool specimens. 1470 61

Helicobacter pylori (H. pylori) is a spiral gram-negative bacterium, characterized by positive urease, catalase and oxidase activity. The complete resolution of the full genome has elucidated the biological characteristics, the pathogenicity, and the bacterial evolution. The infection is acquired in childhood by oral-oral transmission in developed countries, probably an intra-familiar transmission. The infection has an association with chronic histological gastritis, peptic ulcer, gastric cancer and MALT lymphoma in the stomach. All patients with H. pylori infection have histological gastritis and most of them remain asymptomatic for life. Only a minority of the infected individuals occurs ulceration or gastric cancer. Cure of the infection prevents recurrence of peptic ulcer without persistent treatments against ulceration. Concerning gastric cancer, WHO concluded in 1994 that H. pylori is a definite carcinogen in humans on the basis of epidemiological studies. Evidences that the infection leads to the development of gastric cancer have been accumulated in animal models as well as in vitro experimental studies. Such clinical diversities are caused by variations of H. pylori pathogenicity, host susceptibility, environmental factors including foods and those interactions. At present, an eradication treatment of H. pylori, combined with a proton-pump inhibitor and two antibiotics (clarithromycin and amoxicillin) is restrictedly approved in the patients with gastric or duodenal ulcer by Japanese health care system.
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PMID:[What is Helicobacter pylori?: associated diseases in human]. 1510 Nov 86


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