Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Being pepsinogen A (PGA) levels generally reduced and pepsinogen C (PGC) increased in gastric cancer patients, PGA/PGC ratio has been proposed as a useful marker of the tumour. We tested PGA, PGC and Gastrin (G) levels in patients with gastric cancer (39) and, as a control, in patients with epithelial dysplasia (21), chronic atrophic gastritis (57), gastric ulcer (11) or subjects lacking major or minor endoscopic and microscopic changes at gastroscopy (48). PGA and PGA/PGC levels were significantly reduced in gastric cancer patients (p less than 0.005 and p less than 0.0001 respectively with analysis of variance). Gastrin levels were also reduced in the same patients (p less than 0.005). We therefore adopted an index number (PGA x Gastrin) which was also dramatically reduced in gastric cancer (p less than 0.005); using an arbitrarily chosen cut-off, the "marker" showed very high sensitivity (76%), specificity (96%) and overall accuracy (74%, by Youden J test). We therefore suggest the use of the index number PGA x G in the diagnosis of gastric cancer, as the most useful gastrin presently available, to our knowledge.
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PMID:Pepsinogen A/pepsinogen C or pepsinogen A multiplied by gastrin in the diagnosis of gastric cancer? 175 13

It has been reported recently that there was genetic heterogeneity in gastric ulcer disease depending upon the location of the ulcer, and that there was a significant association between the restriction fragment length polymorphism (RFLP) for pepsinogen C (PGC) gene and gastric body ulcer. In the present study, the association of the RFLP for PGC gene with combined gastric and duodenal ulcers was investigated to analyse genetic factors in its aetiology. Eighty unrelated controls and 47 patients with combined gastric and duodenal ulcers were studied. The allele frequencies of the large (3.6 kilobase EcoRI fragment) and the small fragment (3.5 kilobase EcoRI fragment) were, respectively 80.6 and 19.4% in controls, 60.0 and 40.0% in patients with combined gastric body and duodenal ulcers, 69.0 and 31.0% in patients with combined gastric angular and duodenal ulcers, and 81.8 and 18.2% in patients with combined gastric antral and duodenal ulcers. The allele frequency of the small fragment was significantly higher in patients with combined gastric body and duodenal ulcers than in controls. The genotypes that possessed the small fragment were significantly more frequent in patients with combined gastric body and duodenal ulcers (66.7%) than in controls (33.8%) and combined gastric antral and duodenal ulcers (27.3%). These results suggest that there is genetic heterogeneity in combined gastric and duodenal ulcers depending upon the location of gastric ulcer, and that combined gastric body and duodenal ulcers are associated with the small fragment allele of the PGC RFLP in the same way as solitary gastric body ulcers.
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PMID:Genetic heterogeneity of combined gastric and duodenal ulcers detected by pepsinogen C gene polymorphism. 794 14

The human stomach mucosa contains two main group of gastric proteinases. Both pepsinogen A (PGA) and pepsinogen C (PGC) consist of molecular variants, isozymogens, which can be separated electrophoretically, PGA was found to consist of five isozymogens (Pg1-Pg2), and PGC of two isozymogens (Pg6 and Pg7). Five hundred zymograms were examined and electrophoretic mobility of pepsinogens from patients with gastric cancer was found to be higher than from other gastric diseases. The ratio of isozymogens Pg3 to Pg5 differs in to great extent in various disease. Patients with ulcer disease have this value higher than 1, but patients with gastric cancer lower than 1. Patients with gastric ulcer have lower occurrence of Pg1 and SMP in antrum. In patients with gastric carcinoma lower concentration of PGA and also ratio PGA to PGC are observed.
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PMID:Pepsinogen polymorphism in human gastric mucosa in relation to gastric diseases. 799 9

This study was aimed to investigate the association of restriction fragment length polymorphisms (RFLPs) for pepsinogen genes with peptic ulcer disease. Eighty unrelated controls, 61 patients with gastric ulcer, and 57 patients with duodenal ulcer were studied. No genetic polymorphisms for pepsinogen A were detected by EcoRI digestion in Japanese subjects but a 100 base pairs insertion-deletion RFLP for the pepsinogen C gene was observed. The allele frequencies of the large (3.6 kilobase EcoRI fragment) and the small fragment (3.5 kilobase EcoRI fragment) were 80.6% and 19.4% respectively in controls, 55.4% and 44.6% in patients with gastric body ulcer, 79.4% and 20.6% in patients with gastric angular ulcer, 71.4% and 28.6% in patients with gastric antral ulcer, and 75.4% and 24.6% in patients with duodenal ulcer. The allele frequency of the small fragment was significantly higher in patients with gastric body ulcer than in controls and in patients with gastric angular or antral ulcer. The genotypes which possessed the small fragment were significantly more frequent in patients with gastric body ulcer (78.4%) than in controls (33.8%) and in patients with gastric angular or antral ulcer (37.5%). These results suggest that there is a significant association between the genetic polymorphism at the pepsinogen C gene locus and gastric body ulcer, and that the pepsinogen C RFLP is a useful marker of the genetic predisposition to this disorder. These results also indicate genetic heterogeneity of gastric ulcer disease, and suggest that the pepsinogen C RFLP may be a useful subclinical marker to explain the differences in genetic aetiologies of gastric body ulcer and gastric angular or antral ulcer.
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PMID:Pepsinogen C gene polymorphisms associated with gastric body ulcer. 809 9

During the healing of experimental gastric ulcers in the oxyntic mucosa, there is a dedifferentiation of the glands in the ulcer margin: previous studies have shown that the parietal cells lose their capacity to produce HCl, and mucous cells replace the zymogen cells. Primarily, we wished to investigate whether or not the glands of the ulcer margin transcribe mRNA for pepsinogen; secondly we also wanted to locate such transcription in other parts of the gastroduodenal epithelium. For this purpose, we first established the baseline for distribution of pepsinogen mRNA in normal rats. We then studied its location in the margin of ulcers in the corpus region after 1-15 days of healing. Formaldehyde-fixed paraffin sections were used for in situ hybridization of mRNA for pepsinogen C, utilizing radioactive riboprobes. The normal gastroduodenal mucosa showed widespread hybridization: the signal was particularly strong in the zymogen cells; weaker signals were obtained from the mucous neck cells, and the cells of the cardiac, antral, and Brunner glands. Specific hybridization was weak or absent in the ulcer margin during the entire period studied. It is concluded that the capacity to produce pepsinogen C is significantly reduced or absent in the gastric ulcer margin during the first 15 days of healing; this should reduce the risks of peptic attack on the delicate scar and margin tissues during ulcer healing.
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PMID:The expression of pepsinogen c mRNA in normal gastroduodenal mucosa and the gastric ulcer margin of the rat. 885 38

We described gene analysis of acid proteinases, cathepsin E (CTSE), pepsinogen A (PGA), and pepsinogen C (PGC), and demonstrated the clinical significance of these genes. CTSE was highly expressed in pancreatic cancer and can be a tumor marker for pancreatic cancer. PGC gene polymorphism was associated with gastric ulcer and can be a subclinical marker of the genetic predisposition to gastric ulcer.
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PMID:[Gene analysis of acid proteases]. 892 Jun 89