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

Historical review of the pathological investigation on stomach cancer in Japan shows that the central problem had been whether or not gastric cancer developed from chronic peptic ulcer. This theory of ulcer cancer sequence was developed from chronic peptic ulcer. This theory of ulcer cancer sequence was supported by many researchers after the war in the period of 1946-64. Subsequently, systematic studies made at the Cancer Institute revealed that carcinoma arises from the gastric mucosa independently of chronic ulcer. The pathological interest then shifted toward investigation of the histogenesis and biological characteristics of gastric carcinoma. It is concluded that gastric carcinoma can be classified into two types; undifferentiated carcinoma (UCA or gastric type) and differentiated one (DCA or intestinal type). The former arises from the ordinary mucosa and cancer phenotype of this carcinoma resembles to that of the ordinary mucosa, and the latter arises from the metaplastic epithelium of intestinal type showing a cancer phenotype resembling to that of the intestinal metaplastic epithelium. These two carcinomas are also different in biological behaviors, such as growth pattern, invasiveness, metastasis, and prognosis. The frequency of UCA is almost the same in both sexes. DCA, however, occurs more often in male than in female. The time trend data indicates that in both sexes the number of DCA decreased, but that of UCA is steady, so that the ratio of DCA to UCA decreased since 1965. These results combined with the concept of the basic and variable cancer leads to a conclusion that UCA is a basic cancer and DCA is a variable cancer of the stomach.
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PMID:Pathological studies of human gastric cancer. 676 3

The existence of Helicobacter pylori in the biliary tract was investigated. Seven bile samples were included in this study. Among them, six bile samples were collected by percutaneous transhepatic cholangiodrainage and the other by needle aspiration during cholecystectomy. Using nested PCR with two sets of primers homologous to the urease A gene, Helicobacter pylori DNA was detected. Three samples, one from a patient with advanced gastric cancer involving the pancreatic head and two from patients with pancreatic head tumor, were found to be positive for Helicobacter pylori DNA. On the other hand, three samples from patients with cholangiocarcinoma and one from a patient with chronic cholecystitis were all negative. To further verify the specificity of our PCR analysis, partial sequences of the PCR products from the three positive samples were analyzed by direct sequencing. Several silent mutations and a missense mutation (AAA to AGA; Lys-164 to Arg-164) were identified in the urease A gene. We conclude that Helicobacter pylori DNA can be easily detected in the bile samples. The possibility of asymptomatic cholangitis caused by this organism requires further investigation.
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PMID:Detection and partial sequence analysis of Helicobacter pylori DNA in the bile samples. 758 92

Although an association is suggested between gastric cancer and prior infection with Helicobacter pylori (HP), the role of HP in gastric carcinogenesis remains obscure. HP has potent urease activity and produces ammonia, a factor causing HP-related gastroduodenal mucosal lesions. In this study, rats were examined in an effort to determine effects of ammonia on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). After pretreatment with MNNG (83 mg/l) for 24 weeks, a solution of either 0.01% ammonia or plain tap water was administered to the animals as drinking water for an additional 24 weeks. The administration of the 0.01% ammonia solution significantly increased the incidence and number of cancers in the glandular stomach. The numbers of cases in which these cancers penetrated the muscle layer or deeper and of low-grade differentiated adenocarcinomas were significantly higher in rats receiving the ammonia solution. Continuing administration of ammonia accelerated cell proliferation in the gastric mucosa, but had no effect on the serum gastrin level. Therefore, gastric ammonia, which stimulates mucosal cell proliferation, appears to be an important promoter in carcinogenesis in rats and possibly in the HP-related gastric carcinogenesis in humans.
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PMID:Mechanism for ammonia-induced promotion of gastric carcinogenesis in rats. 769 14

Helicobacter pylori in the stomach is an etiological factor of gastritis and peptic ulcer. It is now considered that gastric cancer can be, at least in some cases, a late complication of H. pylori infection. In 123 consecutive endoscopic antral biopsies obtained from patients with the Okamoto Hospital, the specimens were subjected to the rapid urease test (RUT), histology (H&E stain), and culture, for the identification of H. pylori. The results of these methods were compared semi-quantitatively in order to evaluate these detection methods for identifying H. pylori. The results of these methods were found to agree well, with the Spearman's rank correlation coefficient between RUT and culture being 0.90 (P < 0.01) and that between histology and culture being 0.80 (P < 0.01). RUT is considered to be a very simple, sensitive, and highly specific test which enables the endoscopist to diagnose H. pylori infection.
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PMID:Significance of rapid urease test for identification of Helicobacter pylori in comparison with histological and culture studies. 771 9

Gastric infection with Helicobacter pylori activates a mucosal inflammatory response by mononuclear cells and neutrophils that includes expression of cytokines interleukin-1 beta (IL-1 beta), IL-6, tumor necrosis factor alpha, and IL-8. In this study, we analyzed the IL-8 response of human gastric cancer cell lines (Kato III, AGS, and MKN28) to H. pylori infection in vitro. IL-8 mRNA expression was detected by reverse transcription-PCR amplification of RNA extracted from epithelial cells after incubation with different H. pylori wild-type and mutant strains, and IL-8 secretion was measured by an enzyme-linked immunosorbent assay. Exposure to viable H. pylori induced IL-8 mRNA and protein synthesis in all three gastric cell lines but not in nongastric epithelial cell lines. Heat-killed H. pylori and a crude cytotoxin preparation did not induce significant IL-8 secretion. IL-8 mRNA peaked between 2 and 4 h postinfection, and IL-8 protein production was maximal 24 h postinfection. Exposure of gastric carcinoma cells to other gastrointestinal bacteria, such as Pseudomonas aeruginosa, Campylobacter jejuni, and Escherichia coli, but not Campylobacter fetus, induced IL-8 synthesis. Wild-type strains that expressed the vacuolating cytotoxin (Tox+) and a cytotoxin-associated gene (cagA) product (CagA+) induced significantly more IL-8 than did CagA- Tox- strains. However, there was no decrease in IL-8 induction by isogenic mutants of CagA-, Tox-, or Cag- Tox- strains or by a mutant lacking the urease subunits. These results indicate that exposure to H. pylori and other gram-negative organisms that do not colonize the gastric mucosa induces IL-8 production by gastric carcinoma cells in vitro. Although the CagA+ Tox+ phenotype of H. pylori is associated with enhanced IL-8 production by gastric cell lines, other bacterial constituents are clearly essential.
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PMID:Interleukin-8 response of gastric epithelial cell lines to Helicobacter pylori stimulation in vitro. 772 72

In patients with systemic sclerosis peristaltic abnormalities may delay gastric emptying, giving rise to bacterial overgrowth, including possibly Helicobacter pylori (HP). Infection with Helicobacter is an important risk factor for esophageal and gastric diseases, including esophagitis, gastritis and gastric cancer. The purpose of this prospective study was to assess gastric HP infection in patients with systemic sclerosis. In 12 patients with systemic sclerosis the newly introduced breath test with 13C-labelled urea was used for indirect detection of gastric urease activity due to HP infection. Five out of 12 patients gave Helicobacter-positive results (42%); 7 patients were negative for Helicobacter colonization (58%). Thus, the risk for gastric diseases caused by HP infection is enhanced in patients with systemic sclerosis compared with white healthy, asymptomatic persons examined in other studies. Helicobacter-positive patients were treated with 2 x 20 mg omeprazole and 4 x 500 mg amoxicillin over 14 days. Afterwards the 13C-urea breath test was repeated and showed negative results for Helicobacter in all systemic sclerosis patients treated. Dual therapy with omeprazole and amoxicillin therapy effectively eradicated HP. The 13C-urea breath test did not cause any side-effects and is therefore considered to be a non-invasive, non-toxic and safe method for the diagnosis and therapeutic control of Helicobacter-status.
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PMID:Helicobacter pylori in patients with systemic sclerosis: detection with the 13C-urea breath test and eradication. 781 72

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

Helicobacter pylori (Hp) were detected in the dental plaque in 40 patients with peptic ulcer, chronic gastritis or gastric cancer with rapid urease test, anti-Hp fluorescein-labelled antibody staining, bacterial culture and electronic microscopy. At the same time, biopsy specimens from the gastric antrum of these patients were studied with WS staining and rapid urease test to detect Hp. The results show that a great lot of Hps is present in most of the patients' dental plaque. The morphological, biochemical and immunological characteristics of the Hp in the dental plaque are similar to those Hp in the gastric mucosa. The above results reveal that the Hp in the dental plaque may be identical with those in the stomach.
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PMID:[Helicobacter pylori in the dental plaque]. 786 41

Helicobacter pylori (HP) is now recognized as a major etiologic agent of chronic gastritis and peptic ulcer and is recently presumed to be a cofactor in the occurrence of gastric cancer. HP has a high urease activity, which possibly plays a role in the pathogenesis of gastroduodenal diseases. In this paper, the function and the genetic structure of HP urease gene and the restriction fragment length polymorphism (RFLP) among HP strains using a probe of HP urease alpha subunit gene were described. HP urease gene cluster, which included structure genes, regulatory genes and accessory genes was identified and associated with the activity and the assembly. The RFLP pattern of HP tends to be distinct in gastric diseases, 460 bp pattern in gastric ulcer and 1,100 bp pattern in chronic gastritis, by Hae III digestion. HP showing a 460 bp RFLP pattern possessed a relatively high urease activity.
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PMID:[Polymorphism of Helicobacter pylori urease genes and gastric diseases]. 790 20

Helicobacter pylori (H. pylori) is a gram-negative bacillus thought to be involved in such diseases of the upper gastrointestinal tract as gastritis, peptic ulcers, and gastric cancer. Urease is regarded as the factor responsible for the pathogenic nature of this bacterium. Therefore, in our examination of the genetic polymorphism of H. pylori, by means of Southern blotting, we used the urease gene as a probe. The Southern blot patterns of H. pylori isolated from different patients differed greatly, the inter-individual variation being so marked that it allowed approximate distinction between individual patients. The Southern blot patterns of individual strains of H. pylori did not change, even when they were stored and passed from generation to generation in our laboratory. These results suggest that DNA fingerprints with a urease gene probe will be useful in epidemiologically tracing H. pylori infection. Almost all strains of H. pylori isolated from different sites in the stomach of a patient on different occasions showed the same pattern, allowing us to confirm that only one strain of H. pylori was responsible for H. pylori infection in individual patients.
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PMID:A clinico-epidemiological analysis of Helicobacter pylori (H. pylori) by Southern blotting with A urease gene probe. 791 38


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