Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Detection of cancer-associated antigen in feces was performed by ELISA binding inhibition method using monoclonal antibody in 25 patients with gastric cancer, 70 with non-malignant gastrointestinal diseases and 100 healthy individuals. Monoclonal antibodies used were CL-4, PS-9, PS-10 and a "cocktail" of the three. The level of cancer-associated antigens detected in feces was significantly higher in patients with gastric cancer than in healthy individuals. PS-9 and PS-10 were also significantly higher in gastric cancer than in non-malignant gastrointestinal diseases. The positive rates of CL-4 were 62.5% vs 7.0%, PS-9 44.0% vs 3% and PS-10 64.0% vs 7.0% in patients with gastric cancer and healthy individuals. When the cocktail of the three was used, the positive rates increased to 88.0% and 14% in the above two groups and 26.6% in gastritis group. These results indicate that the detection of cancer-associated antigen in feces is of value in diagnosis of gastric cancer.
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PMID:[Detection of cancer-associated antigen in feces of patients with gastric cancer by monoclonal antibodies]. 187 86

Substantial agreement has previously been demonstrated between qualitative and morphometric grading of gastric dysplasia. In the present study, a further attempt is made to quantitatively define the dysplastic changes in relation to associated benign or malignant changes of gastric mucosa. In total, 232 cases were studied and were associated with benign peptic ulcer (89 cases), histologically proven gastric cancer (88 cases), and gastritis-associated mild, moderate, and severe dysplasias (55 cases). The analysis showed that one discriminant function consisting of seven morphometric features is sufficient to separate the regenerative and cancer-associated cases. The classification results obtained on the basis of this discriminant function in both training and testing sets are encouragingly similar, indicating that the classification is reliable. This was further confirmed by the results of the application of this rule in the mild, moderate, and severe dysplasia biopsies (the above-mentioned gastritis-associated cases) used in a previous study. The quantitative analysis permits two grades, instead of three, to be distinguished: low-grade and high-grade dysplasia.
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PMID:Morphometric distinction of low- and high-grade dysplasias in gastric biopsies. 277 40

Mice were housed 1, 2, 4, or 8 per cage for 18 months. The more densely housed groups showed markedly reduced food consumption, slightly decreased mean body weights, and a smaller variance of body weights. Tumour incidence was not affected, but gastritis was more prevalent in the more densely housed groups.
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PMID:Effects on mice of numbers of animals per cage: an 18-month study (preliminary results). 693 56

Esophagogastrostomy is a satisfactory method of restoring continuity of the esophagus with minimal long-term effects on growth and development. Anemia or reflux oesophagitis is not a complication of the operation provided the anastomosis is high in the thoracic cage, i.e., above the level of the aortic arch. Postural gastritis secondary to regurgitation of bile was not seen in our patients. The mortality of the operation is high (33%) but this is due to the small number of patients in whom it is indicated. This contrasts markedly with the results in adults where the mortality in large series has fallen to low levels (13%). Thus, esophagogastrostomy should retain a place in selected patients for the primary treatment of esophageal atresia and the high esophageal stricture.
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PMID:Observations on the role of esophagogastrostomy in infancy and childhood with particular reference to the long-term results and operative mortality. 738 64

De-glycosylation of mucins may expose new tumor-associated core protein epitopes. In this study, to attempt to develop useful markers for gastric cancers, we have purified and de-glycosylated gastric mucin and tried to establish monoclonal antibodies (MAbs). A MAb designated A3D4 among established MAbs was shown to react with gastric cancer with high frequency, but not with normal gastric epithelium. Among normal digestive organs, only the colon and gall bladder were positive for MAb A3D4. The incidence of positivity in gastric cancer was 75% for intestinal-type adenocarcinoma (n = 28), 40% for solid-type adenocarcinoma (n = 5) and 33% for signet/scirrhous-type adenocarcinoma (n = 15). Interestingly, adenoma and intestinal metaplasia (IM) with chronic gastritis or peptic ulcer were negative for MAb A3D4, whereas 8 out of 13 cases (62%) of IM with gastric cancer was positive. Western-blot analysis using the lysate from normal colon tissues revealed a high-molecular-weight (> 300-kDa) smear-like band. Immunohistochemical analysis indicated that the reactivity of MAb A3D4 was clearly increased when tissue sections were pre-treated with periodic acid or O-glycanase, while it was decreased by pre-treatment with trypsin or protease V8. There was no reactivity with the synthetic peptide encompassing the tandem-repeat sequence of MUC2 or MUC3. These data suggest that MAb A3D4 detects a novel gastric-cancer-associated mucin antigen whose epitope may be peptide in nature.
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PMID:A novel gastric-cancer-associated mucin antigen defined by a monoclonal antibody A3D4. 939 54

To determine the transmission route of Helicobacter pylori, one nude mouse was challenged by H. pylori, and then raised with nonchallenged nude mice in a single cage in a sterilized environment with and without exposure to their feces. After coraising for two and four weeks, all mice were killed to determine H. pylori in the stomach, saliva, and feces and to assess gastritis grade. Natural transmission of H. pylori occurred in 50% (2/4) and 70% (7/10) of mice after two weeks and four weeks of coraising when they were exposed to their feces. H. pylori was detected not only in the stomach but also in saliva and feces by PCR of all challenged and transmitted mice. However, no transmission occurred in mice not exposed to feces of a challenged mouse, while sharing food and water in a single cage. These findings suggest that the fecal-oral transmission route is important, at least in the animal model. Serum levels of anti-H. pylori urease IgG of the H. pylori-transmitted mice increased after coraising, and gastritis was observed in the stomach of both challenged and transmitted mice. We conclude that H. pylori bacteria are transmitted through the fecal-oral route from challenged to nonchallenged nude mice, resulting in gastritis.
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PMID:Transmission of Helicobacter pylori from challenged to nonchallenged nude mice kept in a single cage. 1105 15

Previously, we reported the identification and characterization of a novel cancer/testis antigen gene, CAGE(4), that was expressed in various histological types of tumors, but not in normal tissues, with the exception of the testis. To date, molecular mechanisms for the expression of CAGE have never been studied. In our expression analysis, we found that some cancer cell lines did not express CAGE. The expression of CAGE could be restored in these cell lines by treatment with 5(')-aza-2(')-deoxycytidine, suggesting that the expression of CAGE is mainly suppressed by hypermethylation. Bisulfite sequencing analysis of the 16 CpG sites of the CAGE promoter in various cancer cell lines and tissues revealed a close relationship between the methylation status of the CAGE promoter and the expression of CAGE. The transient transfection experiments displayed that the methylation of CpG sites inhibited the CAGE promoter activity in luciferase reporter assays. The methylation of the CpG sites inhibited the binding of transcription factors, shown by a mobility shift assay. A methylation-specific PCR analysis revealed that hypomethylation of the CAGE promoter was present at frequencies of more than 60% in breast, gastric, and lung cancers, and hepatocellular carcinomas, and at frequencies of less than 40% in prostate, uterine cervical, and laryngeal cancers. Promoter hypomethylation was found in chronic gastritis (19/55, 34.5%) and liver cirrhosis (13/22, 59%), but not in normal prostate, normal colon, or chronic hepatitis. These results suggest that the methylation status of the CpG sites of CAGE determines its expression, that the hypomethylation of CAGE precedes the development of gastric cancer and hepatocellular carcinoma, and that the high frequencies of hypomethylation of CAGE, in various cancers would be valuable as a cancer diagnostic marker.
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PMID:Promoter hypomethylation of a novel cancer/testis antigen gene CAGE is correlated with its aberrant expression and is seen in premalignant stage of gastric carcinoma. 1284 80

To understand whether direct transmission of H. pylori occurs from infected mouse to noninfected mouse, the system using a mouse model we developed previously was tested. Six nude mice were challenged with H. pylori inocula; one group consisted of one challenged nude mouse 1 week after inoculation raised with four nonchallenged nude mice in a single cage. For the single cage, a polycarbonate cage or a mesh-floor cage was used. Then three groups were kept in a polycarbonate cage and the other three groups kept in a mesh-floor cage to avoid H. pylori transmission through stool. After coraising for 1, 2, or 3 weeks, all mice were sacrificed to determine the existence of H. pylori in the stomach, saliva, and stool by culture or PCR and H. pylori-associated gastritis. RAPD fingerprinting patterns using different primers of isolated strains from challenged and nonchallenged mice were compared to understand the origin of transmitted strains. During 3 weeks after coraising of H. pylori challenged and nonchallenged mice, H. pylori was detected in the stomachs in 3 of 12 nonchallenged mice in the polycarbonate cage and in 2 of 12 nonchallenged mice in the cage with a steel mesh floor. H. pylori was detected from saliva or stool in two nonchallenged, infected mice in the polycarbonate cage. Moreover, RAPD fingerprinting using different primers of the total five strains isolated from five nonchallenged, infected mice in both cages showed the same pattern and concordance with that of the challenged strain and the strains isolated from challenged mice. It is demonstrated that intimate interaction is the cause of H. pylori transmission via saliva and stool.
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PMID:Direct transmission of H. pylori from challenged to nonchallenged mice in a single cage. 1598 60

Helicobacter pylori produces acute superficial gastritis in nearly all of its human hosts. However, a subset of individuals develops chronic atrophic gastritis (ChAG), a condition characterized in part by diminished numbers of acid-producing parietal cells and increased risk for development of gastric adenocarcinoma. Previously, we used a gnotobiotic transgenic mouse model with an engineered ablation of parietal cells to show that loss of parietal cells provides an opportunity for a H. pylori isolate from a patient with ChAG (HPAG1) to bind to, enter, and persist within gastric stem cells. This finding raises the question of how ChAG influences H. pylori genome evolution, physiology, and tumorigenesis. Here we describe the 1,596,366-bp HPAG1 genome. Custom HPAG1 Affymetrix GeneChips, representing 99.6% of its predicted ORFs, were used for whole-genome genotyping of additional H. pylori ChAG isolates obtained from Swedish patients enrolled in a case-control study of gastric cancer, as well as ChAG- and cancer-associated isolates from an individual who progressed from ChAG to gastric adenocarcinoma. The results reveal a shared gene signature among ChAG strains, as well as genes that may have been lost or gained during progression to adenocarcinoma. Whole-genome transcriptional profiling of HPAG1's response to acid during in vitro growth indicates that genes encoding components of metal uptake and utilization pathways, outer membrane proteins, and virulence factors are among those associated with H. pylori's adaptation to ChAG.
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PMID:The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: evolution during disease progression. 1678 65

There is a gender-related comorbidity of pain-related and inflammatory bowel diseases with psychiatric diseases. Since the impact of experimental gastrointestinal inflammation on the emotional-affective behavior is little known, we examined whether experimental gastritis modifies anxiety, stress coping and circulating corticosterone in male and female Him:OF1 mice. Gastritis was induced by adding iodoacetamide (0.1%) to the drinking water for at least 7 days. Inflammation was assessed by gastric histology and myeloperoxidase activity, circulating corticosterone determined by enzyme immunoassay, anxiety-related behavior evaluated with the elevated plus maze and stress-induced hyperthermia tests, and depression-like behavior estimated with the tail suspension test. Iodoacetamide-induced gastritis was associated with gastric mucosal surface damage and an increase in gastric myeloperoxidase activity, this increase being significantly larger in female mice than in male mice. The rectal temperature of male mice treated with iodoacetamide was enhanced, whereas that of female mice was diminished. The circulating levels of corticosterone were reduced by 65% in female mice treated with iodoacetamide but did not significantly change in male mice. On the behavioral level, iodoacetamide treatment caused a decrease in nocturnal home-cage activity, drinking and feeding. While depression-related behavior remained unaltered following induction of gastritis, behavioral indices of anxiety were significantly enhanced in female but not male mice. There was no correlation between the estrous cycle and anxiety as well as circulating corticosterone. Radiotracer experiments revealed that iodoacetamide did not readily enter the brain, the blood-brain ratio being 20:1. Collectively, these data show that iodoacetamide treatment causes gastritis in a gender-related manner, its severity being significantly greater in female than in male mice. The induction of gastritis in female mice is associated with a reduction of circulating corticosterone and an enforcement of behavioral indices of anxiety. Gastric inflammation thus has a distinct gender-dependent influence on emotional-affective behavior and its neuroendocrine control.
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PMID:Experimental gastritis in mice enhances anxiety in a gender-related manner. 1794 26


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