Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with Helicobacter pylori(H. pylori) is thought to be an important factor in the pathogenesis of gastritis, peptic ulcer and gastric cancer, and the 13C-urea breath test (13C-UBT) is a convenient and non-invasive method for the detection of H. pylori in the stomach. We have examined the sensitivity, specificity and accuracy of 13C-UBT, comparing it with histology. The 13CO2/12CO2 ratio was measured by using infra-red spectroscopy(IR) and gas chromatography/mass spectrometry(GC-MS). The IR analyzer should be particularly useful for the diagnostic test of H. pylori infection using 13C-UBT.
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PMID:[13C-urea breath test]. 1260 18

Infection with Helicobacter pylori has been recognized as a cause of gastric carcinoma. Although the neoplasia is always detected in adults, the infection starts in childhood. It has been reported that early age at first infection is a determinant of gastric cancer risk. In this study, we examined the histopathology of the gastric mucosa in infected children from a population at high risk for gastric cancer (Pasto, Colombia) and compared it with that of a lower-risk population (New Orleans, LA). Gastric biopsies obtained from antrum and corpus were stained with hematoxylin and eosin and Steiner's silver method. Immunohistochemical stains were used to identify B lymphocytes (CD20), T lymphocytes (CD3 and CD8), macrophages (CD68), and polymorphonuclear neutrophil myeloperoxidase. Morphometric techniques were used to evaluate the immunohistochemical stains. In both populations, the inflammatory lesions were seen predominantly in the antrum. Compared with children from the lower-risk populations, children from the higher-risk population exhibited more severe polymorphonuclear neutrophil infiltration, stromal and intraepithelial lymphocyte infiltration, mucus depletion, and H. pylori colonization density. Regenerative activity was significantly more marked in the lower-risk population. Morphometric analysis of immunohistochemical stains showed increased representation of T lymphocytes and macrophages in the higher-risk population. Most T lymphocytes stained positive for CD8, a marker of suppressor/cytotoxic cells. B lymphocytes were relatively more abundant in the lower-risk population. The possibility that the aforementioned characteristics of H. pylori infection in children are related to cancer risk in adults is discussed.
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PMID:Histopathology of gastritis in Helicobacter pylori-infected children from populations at high and low gastric cancer risk. 1267 53

The incidence of gastric cancer in the countries of South East Asia is variable, ranging from age-standardized rates of 20.9/105 (men) and 10.4/105 (women) in Hanoi, Vietnam to 4.1/105 (men) and 2.1/105 (women) in Khon Kaen, Thailand. The reasons for these differences are unknown. Possible explanations are differences in dietary habits, alcohol drinking, smoking and/or the prevalence of infection with Helicobacter pylori (H. pylori). A case-control study was conducted in Khon Kaen, Thailand, to study the role of these factors in gastric cancer carcinogenesis. 131 gastric cancer cases and 262 matched controls were recruited for the study. Information on dietary habits, alcohol drinking and smoking were collected by a structured questionnaire. Blood samples were available from 111 cases and 232 controls for H. pylori assay. Using an unconditional logistic regression model controlling for age and sex, we assessed the effects of dietary habits, alcohol drinking, smoking and H. pylori infection on the risk of gastric cancer. A high intake of salt (OR=1.8; 95%CI 1.1-3.0) and fermented foods (OR=1.9; 95%CI 1.1-3.3) was found to be associated with an increased risk. Preference for spicy food was not associated with gastric cancer risk in this population. Although there were negative associations between gastric cancer and vegetable and fruit intake, they were rather weak (OR 0.8 for both) and non significant. There were also weak (non-significant) associations with smoking and alcohol consumption, and no association with H. pylori infection (OR=0.6; 95%CI 0.4-1.0). Infection of H. pylori was associated with various indicators of crowding.
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PMID:Gastric Cancer: the Roles of Diet, Alcohol Drinking, Smoking and Helicobacter pylori in Northeastern Thailand. 1271 93

Infection with the human microbial pathogen Helicobacter pylori is assumed to lead to invasive gastric cancer. We find that H. pylori activates the hepatocyte growth factor/scatter factor receptor c-Met, which is involved in invasive growth of tumor cells. The H. pylori effector protein CagA intracellularly targets the c-Met receptor and promotes cellular processes leading to a forceful motogenic response. CagA could represent a bacterial adaptor protein that associates with phospholipase Cgamma but not Grb2-associated binder 1 or growth factor receptor-bound protein 2. The H. pylori-induced motogenic response is suppressed and blocked by the inhibition of PLCgamma and of MAPK, respectively. Thus, upon translocation, CagA modulates cellular functions by deregulating c-Met receptor signaling. The activation of the motogenic response in H. pylori-infected epithelial cells suggests that CagA could be involved in tumor progression.
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PMID:Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response. 1271 69

The presence of spiral-shaped micro-organisms in the human stomach was described over 100 years ago by Polish clinical researcher, Professor W. Jaworski at Cracow Jagiellonian University. Their presence was then confirmed in animals by G. Bizzazero, but was not really taken seriously until the late 1970s, when J.R. Warren, a pathologist in Perth, Australia, noted the appearance of spiral bacteria overlaying gastric mucosa, chiefly over inflamed tissue. Warren and B.J. Marshall cultured these organisms in 1982 from 11 patients with gastritis and were able to demonstrate a strong association between the presence of Helicobacter pylori (H. pylori) and the finding of inflammation in gastric biopsies. People, who did not exhibit gastritis, also did not have the organism, a finding which was confirmed in a number of studies. Originally called Campylobacter pyloridis, the name was changed to Campylobacter pylori, and then later to Helicobacter pylori (H. pylori) as specific morphologic, structural, and genetic features indicated that it should be placed in a new genus. Marshall elegantly fulfilled Koch's postulates for the role of H. pylori in antral gastritis with the self administration of H. pylori, and also showed that it could be cured by use of antibiotics and bismuth salts. Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. The role of H. pylori in non-ulcer dyspepsia remains unclear. These practical aspects of H. pylori were subjects of two international symposia organized by us in 1995 and 1997 in Cracow, helping to promote research and Polish consensus regarding treatment of H. pylori infection.
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PMID:Discovery by Jaworski of Helicobacter pylori and its pathogenetic role in peptic ulcer, gastritis and gastric cancer. 1507 63

Gastro-oesophageal reflux disease (GORD) and Helicobacter pylori infection are both common in Western countries. A recently published meta-analysis has shown an association between an absence of H. pylori infection and GORD symptoms. Infection with cagA-positive H. pylori strains is a causative factor for the development of duodenal ulcer and is a risk factor for gastric cancer. Data about a protective role of cagA-positive H. pylori strains against more severe reflux oesophagitis are documented in several studies, but questioned by some other studies. There is a need for further studies to clear the definite role of cagA-positive H. pylori strains in severe reflux oesophagitis and their possible effect on the development of Barrett's adenocarcinoma. The role of Helicobacter pylori in gastro-oesophageal reflux disease (GORD) is still discussed controversially. Different factors might be responsible for the remarkably heterogeneous results of previously performed studies (e.g. location, environmental factors and different virulence factors of H. pylori strains). A very recently published meta-analysis has shown a significant association between the absence of H. pylori infection and GORD symptoms, and a positive correlation between anti-H. pylori therapy and the occurrence of both de-novo and rebound/exacerbated GORD. The results of this meta-analysis are questioned by some authors because of single larger trials and geographical variations of the studies analysed. Data on the role of the cytotoxic-associated antigen (cagA)-positive H. pylori strains are contradictory. Several studies have provided evidence supporting the protecting role of cagA-positive H. pylori strains against GORD, but these results were not confirmed by all studies. A multitude of patients suffer from H. pylori infection and GORD, simultaneously. Therefore, further studies are needed to clearly answer the question whether infection with cagA-positive H. pylori strains, which bear a well-documented risk for gastric cancer and gastro-duodenal ulcer, is really helpful against more severe reflux oesophagitis and, in consequence, perhaps protective against Barrett's oesophagus and Barrett's adenocarcinoma.
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PMID:cagA-positive Helicobacter pylori strains and gastro-oesophageal reflux disease: still puzzling? 1520 76

The human gastric pathogen Helicobacter pylori attaches to antral epithelial cells in vivo. Cultured human antral epithelial cells, AGS and NCI-N87 cell lines, were grown in the absence or presence of H. pylori and compared with respect to gene transcript levels, protein expression, organization of the actin cytoskeleton, and the regulation of cell migration. The Clontech Neurobiology array detected differentially expressed transcripts, while Western blots were used to investigate related changes in protein levels. Infection with H. pylori consistently upregulated annexin II, S100 A7, Rho-GTP, and IQGAP-1, whereas SSTR-1 was downregulated upon H. pylori infection. In the adherens junction, E-cadherin and IQGAP-1 were translocated from the plasma membrane to intracellular vesicles. The primary and NCI-N87 cells were similar with respect to cell-cell and cell-matrix adhesion and cell migratory behavior; in contrast the AGS cells were significantly different from the primary gastric epithelial cell preparations, and thus caution must be used when using this cell line for studies of gastric disease. These studies demonstrate a correlation between H. pylori infection and alterations to epithelial cell adhesion molecules, including increased levels of Rho-GTP and cell migration. These data indicate that destabilizing epithelial cell adherence is one of the factors increasing the risk of H. pylori-infected individuals developing gastric cancer.
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PMID:Helicobacter pylori infection targets adherens junction regulatory proteins and results in increased rates of migration in human gastric epithelial cells. 1532 13

Heat shock proteins (HSPs) are crucial for the maintenance of cell integrity during normal cellular growth as well as during pathophysiological conditions. While functioning mainly as molecular chaperones, HSPs also appear to be involved in diverse biological activities, such as apoptosis, carcinogenesis, and cytoprotection from cytotoxic damage. Infection with Helicobacter pylori causes inflammation in the gastric mucosa, leading to gastritis, gastric ulcers, duodenal ulcer disease, and even gastric cancer, but the role of HSPs in H. pylori-associated gastropathy is not known. Using two-dimensional electrophoretic analysis, we have observed significant shifts in HSP profiles after H. pylori infection in RGM-1 cells. We therefore evaluated the effect of treatments that induce HSPs on H. pylori-induced inducible nitric oxide synthase (iNOS) expression. We found that H. pylori infection significantly attenuated the expression of HSP70, whereas exposure of cells to noncytotoxic heat shock or geranylgeranylacetone restored HSP70 expression, as well as suppressing the expression of iNOS, a major cause of H. pylori-induced gastric tissue damage. Our results suggest that induction of HSP70 confers cytoprotection against H. pylori infection by inhibiting the expression of iNOS. In conclusion, these results provide important insights into the flux in HSPs profiles in response to H. pylori infection and highlight the cytoprotective role of HSP70 in H. pylori infection.
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PMID:Restoration of heat shock protein70 suppresses gastric mucosal inducible nitric oxide synthase expression induced by Helicobacter pylori. 1537 40

Helicobacter pylori (H. pylori) is the principal cause of peptic ulcer disease and important risk factor in gastric cancer. Gastric mucosal biopsy specimens taken from 110 patients were examined by polymerase chain reaction (PCR), culture and urease test. The ureA gene was detected in 52 out of 110 examined samples. The cagA gene was detected in 35 (67.3%) out of these 52 specimens (ureA+). This gene was presented in all of patients with stomach ulcer, in 75.0% of patients with duodenitis, 69.6% of patients with duodenal ulcer and 58.3% of patients with gastritis. H. pylori was detected by culture in 24 (25.3%) out of 95 samples. These results were confirmed by PCR. H. pylori was detected additionally in 20 samples only by PCR. This bacterium was detected more frequently by PCR than by culture (46.3% vs 25.3%). Results obtained by using three methods: culture, urease test and PCR were concordant in 47.0% (39 out of 83 patients). In 16 (19.3%) cases H. pylori was detected by two methods: urease test and PCR. Infection was detected only by PCR in 3 (3.6%) cases and in 25 cases (30.1%) only by urease test.
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PMID:[Comparison of diagnostic methods for Helicobacter pylori detection and identification of cagA gene in clinical specimens]. 1586 38

Helicobacter pylori is a human-specific gastric pathogen that colonizes over half the world's population. Infection with this bacterium is associated with a spectrum of gastric pathologies ranging from mild gastritis to peptic ulcers and gastric cancer. A strong predictor of severe disease outcome is infection with a bacterial strain harbouring the cag (cytotoxin associated gene) pathogenicity island (PAI), a 40 kb stretch of DNA that encodes homologues of several components of a type IV secretion system (TFSS). One gene within the cag PAI, cagA, has been shown to encode a substrate for the TFSS which is translocated into host cells and causes multiple changes in host cell signalling. Here we review recent advances in the characterization of type IV secretion, the activities of CagA and CagA-independent effects of the TFSS, which are contributing to our understanding of H. pylori pathogenesis.
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PMID:Helicobacter pylori-host cell interactions mediated by type IV secretion. 1595 24


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