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

Helicobacter pylori is an important pathogen in humans, causing chronic gastritis and playing a major role in the development of peptic ulcers and gastric cancer. The organism is highly adapted to the human stomach, largely due to its motility and ability to produce large amounts of urease. It binds specifically to the gastric mucosa via adhesion pedestals; colonization of the duodenum only occurs in the presence of gastric metaplasia. Infection with H. pylori leads to gastritis, but the majority of infected patients are asymptomatic, and it is thought that the ability of H. pylori to cause more severe disease may be related to the presence of the cagA gene. With improvements in public health and living conditions, the prevalence of H. pylori infection in developed countries is decreasing, and this is associated with a decline in the incidence of peptic ulcer and gastric cancer.
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PMID:The nature of Helicobacter pylori. 872 98

Recent international consensus statements have concluded that Helicobacter pylori is a causal factor in peptic ulcer disease and a Group 1 carcinogen in humans, and that all patients with peptic ulcer associated with H. pylori infection should receive eradication therapy. There are marked differences in the presentation of peptic ulcer disease between Japanese patients and those from other countries, however, and thus a committee of the Japanese Society of Gastroenterology has been set up to develop guidelines for clinical trials in patients with gastric or duodenal ulcers associated with H. pylori. According to these guidelines, eradication therapy should normally consist of dual therapy with a proton pump inhibitor, such as omeprazole, and an antibiotic; a nitroimidazole can be added, however, if necessary. The diagnosis of H. pylori should be made on the basis of a positive culture of the organism or histological examination of gastric biopsies, together with a positive urease test or 13C-urea breath test. Eradication should be confirmed by the same means 4-6 weeks after treatment. Other research is investigating the relationship between H. pylori and gastric cancer, an important issue in view of the high incidence of this condition in Japan. There is evidence that the Mongolian gerbil may be a useful animal model to investigate this question.
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PMID:Helicobacter pylori in Japan. 872 10

Helicobacter pylori (HP) infection was detected in different segments of the gastric mucosa in 13 patients with stomach tumors. Twenty five patients suffering from stomach ulcers were used as controls. HP infection was diagnosed by means of urease and microbiological testing. HP was identified in all cases of stomach cancer, the rates of dissemination in the mucosa in such patients being higher than in those with stomach ulcers.
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PMID:[Detection of Helicobacter pylori in stomach cancer]. 880 37

Helicobacter pylori infection has been associated with chronic atrophic gastritis, a precursor of gastric cancer. We conducted a prospective, case-controlled study to investigate whether H. pylori infection increases the risk of gastric cancer in Korean people with a high risk of gastric cancer. We enrolled 160 gastric cancer patients who were confirmed by endoscopic biopsy during 1994 and 160 age-matched control subjects with non-ulcer dyspepsia were compared to document the relationship between H. pylori infection and gastric cancer. The presence of H. pylori infection was determined by the rapid urease test and/or histology by Wright-Giemsa staining. The overall presence of H. pylori infection was 60% in gastric cancer patients and 51.9% in age-matched control subjects (odds ratio 1.39; 95% confidence interval 0.894-2.17; P = 0.143). Carcinomas of cardia, body and antrum were not associated with H. pylori infection (odds ratio 1.43, 1.69 and 1.29, respectively; 95% confidence interval, 0.271-7.52, 0.787-3.62 and 0.689-2.43, respectively; P = 0.178, 0.177 and 0.642, respectively) nor was the intestinal or diffuse type of cancer (odds ratio 1.39 and 1.40, respectively; 95% confidence interval 0.791-2.45 and 0.681-2.87, respectively; P = 0.250 and 0.835, respectively). Gender was not a risk for gastric cancer. In contrast to previous studies, these results do not provide evidence of H. pylori infection for gastric carcinogenesis in Korea.
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PMID:Helicobacter pylori infection and the risk of gastric cancer among the Korean population. 908 9

H. pylori infection is strongly implicated in the pathogenesis of peptic ulcer disease and gastric cancer. Although the infection may be detected in over half the world's population, only a proportion will develop either ulcer disease or gastric cancer. The prevalence of the infection is very high in both diseases, but other factors combined with chronic infection must lead to specific clinical manifestations of the disease. Long-standing infection results in chronic active gastritis. In a certain subset of the H. pylori-infected population, factors such as dietary, environmental, and/or genetic factors, or specific strains of the bacterium, may result in the expression of one disease or another. There are now many investigations into these various aspects of association of the infection and disease outcome which may lead to elucidation of the actual processes in the development of specific disease in the H. pylori-infected patient. Many different tests are now available for accurate diagnosis of the infection. The non-invasive tests include the serologic tests, which include both the ELISA and the rapid-immunoassay, and the urea breath test. Invasive tests can be performed on the patient at the time of endoscopy when tissue specimens can be taken for the rapid urease test, histology, or culture.
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PMID:Helicobacter pylori: its role in ulcer disease and gastric cancer and how to detect the infection. 913 57

Helicobacter pylori is associated with primary antral gastritis, duodenal ulceration, and gastric cancer. Current regimens for treating infection in children using bismuth and antibiotics for two to six weeks are cumbersome. The aim of this study was to evaluate a one week course of treatment. All children undergoing endoscopy were assessed for the presence of H pylori by culture, histology, rapid urease test, and 13C urea breath test. Infected children received a one week course of colloidal bismuth subcitrate 480 mg/1.73 m2/day (maximum 120 mg four times a day), combined with metronidazole 20 mg/kg/day (maximum 200 mg three times a day), and clarithromycin 15 mg/kg/day (maximum 250 mg twice a day). To optimise compliance, drugs were dispensed in a 'Redidose' box containing a compartment for each day, and subcompartments marked 'breakfast', 'lunch', 'dinner', and 'bedtime'. Compliance and side effects were assessed immediately after treatment. A urea breath test was performed at least one month after treatment. Twenty two children infected with H pylori were entered into the study; 20 of these took all doses; two children suffered significant side effects (diarrhoea and vomiting). H pylori was eradicated in 21 of the 22 children (95.45%; 95% confidence interval 77% to 100%). This study shows that H pylori infection in children can be cleared by a one week course of treatment.
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PMID:One week treatment for Helicobacter pylori infection. 916 31

Helicobacter pylori (Hp) has strong urease activity and produces a large amount of ammonia in the stomach. In animal studies, ammonia was shown to accelerate cell kinetics of gastric mucosa, and long-term exposure of the stomach to ammonia leads to mucosal atrophy. To understand this process, we examined the effects of ammonia on the growth and cell cycle progression of human gastric cancer cell lines (HGC-27, MKN1, MKN45) using flow-cytometric analysis. In each cell line, ammonia inhibited the cell growth in a dose-dependent manner and caused significant accumulation of S-phase cells at a cytostatic dose. DNA synthesis of HGC-27 cells treated with ammonia was also suppressed to about 50% of that of the untreated cells. Similar effects were observed on addition of ammonium chloride at the same concentration, while adjusting the pH of the media with NaOH alone to that with the cytostatic dose of ammonia did not affect the cell cycle progression. These observations indicate that ammonia induces S-phase arrest in gastric cells independently of pH.
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PMID:Ammonia inhibits proliferation and cell cycle progression at S-phase in human gastric cells. 924 35

Helicobacter pylori has been established as the major causative agent of human active gastritis and is an essential factor in peptic ulcer disease and gastric cancer. The mechanism that has been proposed for H. pylori to control its inhospitable microenvironment happens to coincide with the pH control technique developed by us. This technique was developed to separate an acidic environment from a basic environment for a sequential enzymatic reaction by the hydrolysis of urea within a thin layer of immobilized urease. In this paper, a mathematical model is presented to consider how H. pylori survives the gastric acidity. The computed results explain well the experimental data available involving H. pylori.
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PMID:Helicobacter pylori survival in gastric mucosa by generation of a pH gradient. 925 24

Helicobacter pylori infection in humans is linked to gastritis, gastric and duodenal ulcers, and gastric cancer. Peptic ulcer disease, as distinct from chronic asymptomatic infection, is strongly associated with expression of bacterial virulence markers, including a major antigen, CagA, and the vacuolating cytotoxin VacA. We have previously described significant differences in colonization rates, independent of socioeconomic status, among ethnic groups in New Zealand. To evaluate relative risks for peptic ulcer disease, we examined the frequency of two virulence markers in H. pylori strains infecting these ethnic groups. Although these markers occurred significantly more frequently in strains isolated from Polynesians than in strains from Europeans, this frequency was not reflected in the incidence of peptic ulcer disease in the two groups. DNA fingerprinting of the urease gene showed that Polynesians are more frequently infected by a group of strains which are genetically distinct from those affecting European New Zealanders. Our data suggest that separate bacterial lineages may have evolved in parallel with race-specific specialization.
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PMID:Evidence for ethnic tropism of Helicobacter pylori. 928 41

Helicobacter pylori infection and adenomatous polyposis coli (Apc) gene mutations have been linked to gastric cancer in humans, but possible synergistic interaction(s) between these risk factors have not been examined. Fourteen C57BL/6 wild-type and 14 Apc1638 heterozygous mice were inoculated with Helicobacter felis at 6 weeks of age and compared at various time points with a similar number of uninfected control mice of the same genotype. Both infected and uninfected Apc1638 mice had a limited incidence of atypical proliferation foci in the mucosa of the antrum and pyloric junction at 4.5 and 6 months of age, whereas polyps of the antrum and pylorus were present in all mice, regardless of infection status, at 7.5 months. In contrast, no altered gastric mucosal foci were observed in control or infected C57BL/6 mice at any time point. Interestingly, the infected Apc1638 mice had less epithelial proliferation and inflammation in the body of the stomach, lower anti-H. felis serum IgG antibody responses (although both the wild-type and Apc mutant mice had a Th1-like immune response, based on a predominantly IgG2a immunoglobulin response), and higher bacteria and urease scores than did infected wild-type C57BL/6 mice. In conclusion, the Apc1638 truncating mutation leads to gastric dysplasia and polyposis of the antrum and pyloric junction, but H. felis infection of the Apc mutant mouse does not lead to an increased rate of gastric neoplasia. In addition, our data suggest this Apc mutation may actually lead to decreased immune, inflammatory, and gastric hyperplastic responses to Helicobacter infection, suggesting the possibility of a novel role for this tumor suppressor gene in the immune and local tissue responses to gastric bacterial infection.
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PMID:Mice carrying a truncated Apc gene have diminished gastric epithelial proliferation, gastric inflammation, and humoral immunity in response to Helicobacter felis infection. 930 81


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