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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathology of gastritis associated with Helicobacter pylori infection is summarized. The literature is reviewed regarding the role of H pylori in the pathogenesis of gastric carcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. The potential mechanisms of gastric carcinogenesis include transformation of the gastric mucosa by metabolic products of H pylori, transformation of the host cell by incorporation of H pylori DNA and genotoxic effects of the inflammatory response to the organism. A model for gastric carcinogenesis is proposed in which H pylori causes cell proliferation, and the risk of DNA damage is increased, leading to inadequate repair and malignant transformation. Investigation of early gastric carcinomas concluded that two main pathways operated in gastric carcinogenesis, both starting from H pylori gastritis and leading to phenotypically variable gastric or intestinal tumour growth. The histological features and molecular genetics of MALT lymphoma are briefly reviewed. There is evidence that tumour cells of low grade B cell MALT lymphoma proliferate specifically in response to H pylori. This response is dependent on T cell activation by H pylori. A proposed model for the pathogenesis of MALT lymphoma postulates that B lymphocytes with a genetic change acquire a growth advantage resulting in a monoclonal proliferation in response to H pylori-activated T cells. Further genetic changes may result in escape from T cell dependency.
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PMID:Role of Helicobacter pylori in the pathogenesis of gastric carcinoma and progression of lymphoid nodules to lymphoma. 1033 33

Bile reflux into the stomach has been considered carcinogenic. Secondary bile acids, and in particular deoxycholic acid, have been shown to act experimentally as co-carcinogens in the colon and are increased in patients with colorectal adenocarcinoma. No information is available with respect to biliary bile acid composition in patients with gastric cancer. We studied biliary bile acid composition in 11 patients with gastric cancer and 23 healthy controls. Bile acids were measured using high-performance liquid chromatography. The site of gastric cancer was the antrum in 6 patients and body in 5. There were 6 intestinal-type and 5 diffuse adenocarcinomas. Only 2 patients had Helicobacter pylori infection. Deoxycholic acid constituted 24% +/- 2% of biliary bile acid in gastric cancer patients versus 22% +/- 2% in healthy controls (NS). Similarly, no differences were found between the two groups for all other bile acids. Deoxycholic acid constituted 23% +/- 3% of biliary bile acid (NS vs. controls) in patients with antral adenocarcinoma and 25% +/- 2% (NS vs. controls) in patients with intestinal-type gastric adenocarcinoma. Gastric adenocarcinoma is not associated with an increase in the more-toxic secondary bile acids, and deoxycholic acid in particular. This reduces the importance of bile acid composition as a promotor in gastric carcinogenesis.
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PMID:Biliary bile acid composition in gastric cancer. 1035 64

The effect of Helicobacter pylori infection on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric cancer was studied using a Mongolian gerbil model. Five-week-old male Mongolian gerbils were divided into four groups of 25-30 animals each and challenged for 20 weeks with H.pylori, MNNG, a combination of H.pylori and MNNG, or neither of them. Four to 20 animals from each group were killed at 16, 24 and 52 weeks after H.pylori inoculation, and histopathological changes in their stomachs were examined. A well-differentiated adenocarcinoma was first observed 24 weeks after inoculation in the combination group. At 52 weeks, only six of 15 animals were colonized with H.pylori persistently, and four of them showed well-differentiated adenocarcinomas; on the other hand, neither of the animals with disappearance of H.pylori from the combination group showed adenocarcinoma. At the same observation time, three of 17 animals from MNNG group showed poorly differentiated adenocarcinomas. The incidence of gastric carcinoma in the combination group was significantly higher than that in the MNNG group (P < 0.05). However, no tumors were seen in the control and H.pylori groups. The present findings demonstrate that H.pylori infection enhances the carcinogenic action of MNNG.
Carcinogenesis 1999 Jul
PMID:Effect of Helicobacter pylori infection on the N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric carcinogenesis in mongolian gerbils. 1038 99

Recent studies (K. Komoto et al., Am. J. Gastroenterol., 93: 1271-1276, 1998) have shown that Helicobacter pylori infection is associated with gastric cancer. However, the mechanism of H. pylori in carcinogenesis has not been clarified. H. pylori infection leads to a sustained production of reactive nitrogen species that may contribute to cause DNA damage. In this study, we examined the expression of inducible nitric oxide synthase (iNOS) and nitrotyrosine in gastric mucosa. The expression of iNOS and nitrotyrosine was examined by immunohistochemistry in 93 patients who initially underwent gastric biopsies between 1975 and 1992. Thirty-four individuals were later found to have gastric cancer at least 2 years after the initial biopsies (group A). The other 59 subjects have shown no evidence of gastric cancer during long-term follow-up. Fifty-one of these patients were positive for H. pylori (group B), and eight were negative for H. pylori (group C). The expression of iNOS and nitrotyrosine in the gastric mucosa was significantly higher in H. pylori-positive groups A and B than in H. pylori-negative group C. Among the H. pylori-positive patients, the expression of iNOS and nitrotyrosine was significantly higher in group A than in group B. These results suggest that high production of iNOS and nitrotyrosine in the gastric mucosa infected with H. pylori may contribute to the carcinogenesis of gastric cancer.
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PMID:Enhanced expression of inducible nitric oxide synthase and nitrotyrosine in gastric mucosa of gastric cancer patients. 1038 26

Helicobacter pylori infection is associated with gastric adenocarcinoma. However, the mechanisms of this interaction are still unclear. This study was conducted to explore the effects of H. pylori infection on early and late stage gastric carcinogenesis. This study included 134 patients with adenocarcinoma of the stomach (ACS), 67 patients with chronic atrophic gastritis (CAG), and 65 normal controls recruited at Memorial Sloan-Kettering Cancer Center (MSKCC) from November 1, 1992 to November 1, 1994. Epidemiologic data were collected by a modified National Cancer Institute Health Habits History Questionnaire. H. pylori infection was diagnosed by pathological evaluation. Risk factors were analyzed using logistic regression. The odds ratio (OR) associated with H. pylori infection was 10.4 [95% confidence interval (CI): 2.6-41.6] for CAG and 11.2 (95% CI: 2.5-50.3) for gastric cancer in comparison with normal controls, with adjustment for pack-years of smoking, alcohol drinking, body mass index, total caloric intake, dietary fat and fiber intake, and Barrett's esophagus. But H. pylori infection was not associated with risk of stomach cancer when patients with stomach cancer were compared with patients with CAG (OR = 0.6, 95% CI: 0.3-1.3) after controlling for potential confounding variables. This association was persistent when only patients with both gastric cancer and chronic gastritis were considered as cases and patients with CAG were considered as controls (OR = 0.7, 95% CI: 0.3-2.0) in the multivariate analysis. Our results suggest that H. pylori infection may be involved in the early stage of development of CAG, but not in the development of stomach cancer from CAG, and indicate that strategies for prevention of stomach cancer should target the early stage to eliminate H. pylori infection in high-risk populations.
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PMID:Helicobacter pylori infection on the risk of stomach cancer and chronic atrophic gastritis. 1046 87

The role of Helicobacter pylori in the carcinogenesis of the stomach has been recognised both in intestinal and diffuse forms. The occurrence of the bacterium was studied in this report, with various methods in biopsy samples from the cancerous stomach, as well as the presence of associated gastritis and metaplasia related to the histological type. Retrospective histological examination were performed on endoscopic biopsy samples from 124 patients with distal stomach cancer using haematoxillin-eosin and Giemsa staining and immunohistochemical tests. Out of the 124 samples 69 (55.64%) was positive: 48 with Giemsa staining and further 21 samples showed immunohistochemical positivity on atrophic gastritis samples despite negative Giemsa staining. In view of the presence of gastritis and metaplasia significant difference (p < 0.001) was found between the positive and negative cases. The ratio of the Helicobacter pylori positive samples was high both for intestinal and diffuse type carcinomas. Our results suggest that the presence of Helicobacter pylori infection is important in the development of both types of carcinoma, nevertheless, the hystological type of the tumor is also decisively influenced by the onset of action of other more direct local eliciting factors.
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PMID:[Detection of Helicobacter pylori in tissue samples of stomach cancer]. 1050 22

It is well known that Helicobacter pylori is able to colonize the gastric mucosa, causing a chronic and persistent infection with complications, such as peptic ulcer and gastric cancer. This review places emphasis on some epidemiological aspects of Helicobacter pylori infection and its mode of transmission. At the same time, invasive and non-invasive methods of diagnosis of Helicobacter pylori infection are illustrated. More space is devoted to the host response following invasion of the stomach. In this respect, the role played by different growth factors and polyamines in the course of Helicobacter pylori disease is discussed also in relation to the result of eradicating treatment. On the other hand, an accurate description of the host immune responses against Helicobacter pylori organism and/or their components (e.g. lipopolysaccharides) is reported. Finally, since Helicobacter pylori has been classified as a class I carcinogen, current researches are focussed on the Helicobacter pylori-induced carcinogenesis.
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PMID:Helicobacter pylori infection and host cell responses. 1058 13

Although epidemiological studies strongly suggest an association between Helicobacter pylori infection and gastric carcinogenesis via a multistage process, a causal link between them has not been demonstrated. We evaluated the endoscopic and histological changes of gastric adenoma, which is considered a premalignant condition, after eradication of H. pylori. Thirty-five H. pylori-infected patients with gastric adenoma were treated with triple therapy (lansoprazole 30mg/day, clarithromycin 400mg/day, and amoxicillin 1500 mg/day) for 1 week. Of these 35 patients, 30 (86%) exhibited no H. pylori by culture or histology after the therapy. Of the 30 gastric adenomas, 7 decreased in size endoscopically; three gastric adenomas especially showed apparent remission, although histological cure in these three patients was not apparent. Our results suggest that removal of H. pylori infection may only mask a gastric adenoma endoscopically owing to the change around the gastric mucosa.
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PMID:Endoscopic and histological reversibility of gastric adenoma after eradication of Helicobacter pylori. 1061 74

Although the advancement of molecular oncology in gastric cancer lags behind that of colorectal cancer, the rapid developments witnessed in recent years have improved our understanding of the carcinogenesis, aetiology, progression and metastasis of gastric cancer. The different molecular genetic alterations in intestinal and diffuse types of gastric cancer have further supported the concept that these two pathological types are different disease entities. The association of telomerase and cadherin changes with Helicobacter pylori infection reinforces its aetiological role. The mutated cadherin gene identified in familial gastric cancer has shone light onto the pathogenesis. Adhesion molecules have already been applied to daily clinical practice as prognostic markers. Future molecular studies will contribute to the screening, classification, disease monitoring and therapeutics of gastric cancer.
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PMID:Molecular biology of gastric carcinoma: from laboratory to bedside. 1063 50

The role and significance of microsatellite instability (MSI) in gastric carcinogenesis remain unknown. This study determined the chronology of MSI in gastric carcinogenesis by examining intestinal metaplasia (IM) from patients with and without gastric cancer. DNA was obtained from gastric specimens of 75 patients with gastric IM (30 cancer, 26 peptic ulcer, and 19 chronic gastritis patients) and was amplified with a set of eight microsatellite markers. Eight (26. 7%) tumors and seven (9.3%) IM samples (three from cancer-free patients) displayed high-level MSI (three or more loci altered). Low-level MSI (one or two loci altered) was detected in 50% of the tumors, in 40% of IM samples coexisting with cancer, and in 38% of IM tissues of cancer-free individuals. Among the 30 cancer patients, microsatellites were more frequently altered in IM coexisting with tumors that showed MSI (P = 0.003). In addition, patients with low-level MSI in the tumor tissues were more likely to have active Helicobacter pylori infection than those with stable tumors (P = 0.02). In conclusion, this study indicates that MSI occurs not only in gastric IM of patients with gastric carcinoma, but also in IM of cancer-free individuals. These data suggest that the progressive accumulation of MSI in areas of IM may contribute to gastric cancer development, representing an important molecular event in the multistep gastric carcinogenesis cascade.
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PMID:Microsatellite instability in gastric intestinal metaplasia in patients with and without gastric cancer. 1066 83


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