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)

Peripheral blood monocytes from healthy subjects, patients with gastric precancer disease (chronic gastric ulcer, stomach polyps and chronic atrophic gastritis) and different stages of gastric cancer were used. Spontaneous and lipopolysaccharide (LPS)-stimulated TNF-like factors production by monocytes was significantly higher in the precancer gastric disease patients than in the healthy subjects. At the same time the spontaneous capacity of monocytes to produce NTF-like factors was 2.5 lower in the gastric cancer patients compared to the healthy subjects. Moreover, in 5/13 of the gastric cancer patients in TNF-like factors production by the LPS-stimulated and non-stimulated monocytes was 1 unit/ml less. Spontaneous and reactive CL indexes were higher in the cancer patients monocytes than in the healthy subjects. The obtained results suggest that reactive oxygen species production can be an alternative mechanism by which a cytotoxic action of monocytes is regulated.
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PMID:[Changes in the profile of cytotoxic mediator monocytes in patients with cancer and precancerous conditions of the stomach]. 185 63

A case of far advanced gastric cancer with multiple liver metastasis (H3) was treated with transarterial intermittent chemotherapy (5-FU: 250 mg/week, Farmorubicin: 10 mg/4 weeks, MMC: 4 mg/2 weeks) and intradermal administration of low molecular lipopolysaccharide (LPSp) extracted from Pantoea agglomerans. The CT examination and endoscopy showed regression of the tumor and the patient was discharged from the hospital. LPSp was given at the concentration of 0.1 microgram initially, and the dose was gradually increased. Finally, the dose of LPSp was increased up to 70 micrograms. No serious side effect except fever was observed. The serum TNF-alpha levels were elevated and, histologically, CD 8(+) lymphocyte dominantly infiltrated around the tumor. These findings clearly indicated the immunological anticancer effect of LPSp. Intradermal administration of LPSp is a promising new adjuvant therapy to improve QOL without serious side effect.
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PMID:[A case report of far advanced gastric cancer with multiple liver metastasis (H3) treated with transarterial intermittent chemotherapy and intradermal administration of low molecular lipopolysaccharide (LPSp) extracted from Pantoea agglomerans]. 757 94

Despite the fact that the inflammatory and immune responses have evolved to combat microorganisms, the present generation of inflammation researchers has evinced relatively little interest, with the exception of septic shock, in microbially-induced inflammation. This in spite of the fact that the Gram-negative cell wall constituent, lipopolysaccharide, has been widely used as a tool in inflammation research. The reason for such lack of interest has been due to the therapeutic efficacy of antibiotics which are the treatment of choice for infections and their inflammatory sequelae. However, this is likely to change within the next decade or so, with the relentless increase in the incidence of antibiotic-resistant strains of bacteria. This will return therapy to the stage where clinicians will have to treat the inflammatory symptoms of infection. Many of these symptoms are due to the stimulation of cytokine synthesis. The capacity of bacteria to induce cytokine synthesis has, until the past few years, centred exclusively on lipopolysaccharide. However, it has been established during the past 5-10 years that a range of other molecules, mainly associated with the surface of bacteria, have the capacity to induce cytokine production. Some of these are exquisitely potent stimulators of pro-inflammatory cytokine synthesis. The nature and mechanism of action of these various cytokine-inducing molecules, for which we have devised the name modulins, is the subject of this review. It is clear that bacteria still have many surprises for us, as exemplified by the recent discovery of the role played by Helicobacter pylori in gastritis, gastric ulceration and gastric cancer.
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PMID:Modulins: a new class of cytokine-inducing, pro-inflammatory bacterial virulence factor. 765 92

Intact Helicobacter pylori cells, as well as cellular components, stimulated nitric oxide (NO) synthesis in an in vitro murine macrophage system by the L-arginine-nitric oxide pathway. Macrophage-mediated NO formation was dependent on the presence of H. pylori and exhibited a dose-dependent increase at H. pylori concentrations between 10(6) and 5 and 10(7) cells/ml. H. pylori mediated NO synthesis also required L-arginine and was inhibited by NG-monomethyl-L-arginine (NMMA), a selective inhibitor of nitric oxide synthase. NO synthesis was induced by whole H. pylori cells. H. pylori media filtrate, extracted membrane proteins, and H. pylori lipopolysaccharide (LPS). Maximal NO synthesis was induced by viable H. pylori cells with media filtrate and membrane protein extracts inducing significant NO responses. NO stimulation by media filtrate and membrane protein extracts support secreted H. pylori products as potential activators of inflammatory cell NO synthesis in vivo. NO synthesis in response to H. pylori suggests that chronic H. pylori infection may increase endogenous formation of NO. Elevated NO exposure may represent an etiologic factor explaining the epidemiologic association between long-term H. pylori infection and gastric cancer.
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PMID:Induction of nitric oxide synthesis in murine macrophages by Helicobacter pylori. 860 78

Infection with Helicobacter pylori plays a crucial role in the etiology of atrophic gastritis and gastric cancer. Studies suggest a nine-fold increased risk for both conditions in the presence of infection. The risk of atrophic gastritis in the presence of infection is dependent upon the severity of the gastritis. Gastritis is increased in subjects infected with a cytotoxic H pylori strain and in those with a decreased acid production. The development of atrophy may be related to the induction of cross-reacting antibodies recognizing Lewis epitopes on H pylori lipopolysaccharide and gastric mucosa. Future studies have to demonstrate whether atrophic gastritis and gastric cancer can be prevented by early H pylori eradication.
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PMID:Helicobacter pylori and atrophic gastritis. 920 81

We have examined the antibody response to Helicobacter pylori lipopolysaccharide (LPS) during natural infection in humans. The sera of over 70% of H. pylori-infected individuals were found to contain immunoglobulin G antibodies against the LPS fractions isolated from smooth strains of H. pylori but not against those derived from rough strains, as determined by enzyme-linked immunosorbent assay. These results taken together with the immunoblot data indicated that the polysaccharide region of H. pylori LPS is antigenic in humans. However, the antigenicity of the polysaccharide varied, depending on the strain. We found that smooth H. pylori strains isolated from the tumors of patients with gastric cancer showed significantly lower antigenicity than smooth strains derived from patients with chronic gastritis and gastric and duodenal ulcers. The results suggest that the levels of antigenicity of the polysaccharide region of H. pylori LPS in humans correlate with the nature of the gastroduodenal diseases and that they allow a particular distinction to be made between gastric cancer and other gastroduodenal diseases, especially chronic gastritis.
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PMID:Low antigenicity of the polysaccharide region of Helicobacter pylori lipopolysaccharides derived from tumors of patients with gastric cancer. 928 13

Helicobacter pylori is a bacterial pathogen, estimated to infect half the world's population. The bacterium is the aetiological cause of gastritis, the common precursor for peptic ulcer disease and gastric cancer. Immunisation of at-risk individuals is the most cost-effective means of dealing with such a widespread pathogen. Potential vaccine candidates need to be identified and characterised. Conventional silver staining is commonly used for the sensitive detection of bacterial protein components separated by SDS-PAGE. Modified silver stains employing periodate oxidation have also been developed for the analysis of purified bacterial lipopolysaccharide. By using these methods in parallel, as a dual silver stain, bacterial fractions can be characterised in terms of protein and LPS content. Strain differences can also be readily identified by comparing protein and LPS profiles. When combined with differential immunoblotting, the dual silver stain is a useful analytical tool for characterising potential vaccine candidate antigens.
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PMID:Dual silver staining to characterise Helicobacter spp. outer membrane components. 944 30

We have evaluated the use of proteinase K (PK)-treated cells isolated from Helicobacter pylori as lipopolysaccharide (LPS) antigens in an immunoblot assay and an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of H. pylori infection. The sera from patients with chronic gastritis, gastric ulcer, duodenal ulcer or gastric cancer, and from healthy adults with or without H. pylori infection were assayed with three commercial serodiagnostic kits (HM-CAP, Helico-G, and G.A.P. II) and novel methods relying on the use of PK-treated cells. The PK-treated cells used in these assays were selected on the basis of their possibility to possess a common epitope in the O-polysaccharides of H. pylori, which is known to be highly immunogenic in humans. Of the sera from these patients, 71-94% were positive with the commercial kits, 97% with immunoblot assay, and 90% with ELISA. On the other hand, of the healthy adults infected with H. pylori, 72-97% were positive with the commercial kits, 86% with immunoblot assay, and 72% with ELISA. PK-treated cells that did not contain the common epitope were unsuitable as an antigen for immunoblot assay or ELISA. Furthermore, the reactivity of these sera reacted specifically with H. pylori PK-treated cells but not with LPSs from other gram-negative bacteria, such as Campylobacter, Proteus, Bordetella, and Salmonella. These results demonstrate that the serological assays relying on the use of H. pylori PK-treated cells possessing a highly antigenic epitope are potentially useful as a serodiagnostic test for H. pylori infection.
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PMID:Utilization of proteinase K-treated cells as lipopolysaccharide antigens for the serodiagnosis of Helicobacter pylori infections. 971 4

Monoclonal antibodies (MAbs) that inhibit adhesion of Helicobacter pylori to human gastric cancer (MKN45) cells were established to clarify the mechanism of adhesion of H. pylori. Of 53 hybridoma clones screened by the primary inhibition assay for adhesion, MAb A20 of IgM class was selected on the basis of both its reactivity to whole cells of H. pylori by ELISA and its inhibitory effect on adhesion of H. pylori. The adhesion of H. pylori strain TK1029 to MKN45 cells was inhibited by MAb A20, depending on the concentration of the MAb. The MAb recognised the surface antigen, lipopolysaccharide (LPS) of H. pylori, suggesting that LPS is associated with adhesion of H. pylori to human gastric epithelial cells.
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PMID:Establishment and characterisation of a monoclonal antibody to inhibit adhesion of Helicobacter pylori to gastric epithelial cells. 987 69

Helicobacter pylori shows a rather high variability of several biochemical markers including lipopolysaccharide structures. This study aimed to determine whether Helicobacter pylori has a potential for phenotypic variability and to describe its effects on bacterial pathogenesis. From colonies of three clinical strains of Helicobacter pylori with rough (R) colony morphology, spontaneous phenotypic variants with smooth (S) colony morphology were isolated that occurred with a frequency of 10(-2) to 10(-3), irrespective of growth conditions. R-variant bacteria produced exclusively low-molecular-mass lipopolysaccharide. They exhibited increased lysis in the presence of plain air. In contrast, the S variants produced low- and high-molecular-mass lipopolysaccharide and did not exhibit increased lysis in the presence of plain air. Cocultivation of bacterial cells with AGS stomach cancer cells revealed that R-variant bacteria but not S-variant bacteria effected an inhibition of high molecular-weight glycoprotein biosynthesis and secretion by the host cells. Skirrow supplement added as selective agent to liquid and/or solid media was tolerated to a similar extent among R- and S-variant bacteria, while all variants proved sensitive to metronidazole, amoxicillin and clarithromycin except for the R and S isolates of strain Hp57, which showed resistance to the latter compound. It was concluded that R- and S-variants of Helicobacter pylori may have distinct roles in pathogenesis; nevertheless, these bacteria may be isolated by traditional methods and eradicated by conventional anti-infective therapy.
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PMID:Growth characteristics and influence of antibiotics on rough/smooth phenotypic variants of Helicobacter pylori. 1048 26


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