1,721,011 research outputs found
IMMUNOHISTOCHEMICAL EVIDENCE OF P53 OVEREXPRESSION IN GASTRIC EPITHELIAL DYSPLASIA
No full textMolecular abnormalities of the p53 gene in chromosome 17p may be among the most commonly observed in human cancer. Their role in gastric carcinogenesis is suggested by their frequent detection in invasive adenocarcinomas. To investigate the chronology with which these abnormalities appear in the gastric carcinogenesis process, the expression of p53 proteins was investigated in late stages of the process, namely dysplasia, and in superficial carcinomas. A polyclonal antibody, CM-1, against both wild-type and mutant proteins was applied to paraffin-embedded biopsy and gastrectomy specimens previously fixed in buffered formalin. Positive nuclear stain was obtained in 36.4% of 33 cases of gastric epithelial dysplasia, corresponding to 19% of mild, 27.3% of moderate, and 64.3% of severe dysplasias. Eight of 13 (61.5%) invasive carcinomas showed positive stain. The data indicate an increased incidence of p53 abnormalities in the late stages of gastric carcinogenesis
Helicobacter pylori genotypes influence serum pepsinogen C levels.
No full textBACKGROUND:
Infection from Helicobacter pylori significantly influences pepsinogen A (PGA) and C (PGC) levels in serum. Increased PGA and PGC serum levels are observed in H. pylori positive patients, while a significant decrease is observed after eradication. Little is known about the relative role of H. pylori cytotoxic strains in this phenomenon. The aim of our study was to assess the influence of cagA genotype on circulating levels of PGA and PGC.
MATERIALS AND METHODS:
We studied 81 consecutive H. pylori positive patients, 64 H. pylori negative patients and 18 healthy controls. H. pylori was evaluated histologically in two antral and two body biopsies (Giemsa and/or Warthin Starry staining). Extracted DNA was then submitted for PCR amplification of both the urease A and cagA genes. A serum obtained from each patient before endoscopy was used for specific radioimmunoassay measurement of PGA and PGC.
RESULTS:
The urease A gene was found in all H. pylori positive patients, the cagA gene was detected in 55 H. pylori positive patients and in none of the H. pylori negative patients. PGA and PGC levels were significantly higher in H. pylori positive than in H. pylori negative patients. A significant association was found between cagA and raised serum PGC levels in patients with antral gastritis but not in patients with peptic ulcer. Serum PGA levels were not affected by cagA.
CONCLUSIONS:
Our results indicate that cagA positivity may influence the circulating PGC levels, probably because it causes a higher grade of mucosal inflammation
Helicobacter pylori (HP) eradication does not influence the natural history of gastric precancerous changes
No full text
LIPID-PEROXIDATION AND ANTIOXIDANT DEFENSE IN HUMAN GASTRIC- MUCOSA - EFFECT OF HELICOBACTER-PYLORI
No full text
GASTRIC EPITHELIAL DYSPLASIA - A PROSPECTIVE MULTICENTER FOLLOW-UP-STUDY FROM THE INTERDISCIPLINARY-GROUP-ON-GASTRIC- EPITHELIAL-DYSPLASIA
No full textTo assess the evolution of gastric epithelial dysplasia (GED), a prospective multicenter study was based on a protocol of repeated endoscopies and biopsies. To date, 134 cases (0.4% of all patients endoscopically examined in the same period) have been diagnosed as having GED and 80 of those have had an "adequate" follow-up (at least three endoscopies). Mean follow-up time was 18 months. Gastric epithelial dysplasia was mild in 59% of cases, moderate in 25%, and severe in 10%. Six percent of the patients had lesions that were "indefinite for dysplasia." Chronic atrophic gastritis (40%), gastric ulcer (32%), gastrectomy (10%), and polyps (9%) were the most frequently associated lesions. The term "regression" was adopted for GED no longer detectable during follow-up and the term "progression" was used when more severe changes or cancer was detected. Mild GED regressed in 66% of cases, persisted in 15%, and progressed in 19% (three cases to moderate, one to severe, and five to cancer). Moderate GED regressed in 30% of patients, persisted in 30%, and progressed in 40% (one to severe GED and seven to cancer). Severe GED regressed in 12.5% of patients, persisted in 12.5%, and progressed to cancer in 75%. Of the five patients with lesions indefinite for dysplasia, two had no dysplastic changes at follow-up and three had cancer diagnosed. Ten of 21 cases of cancer (48%) were at the early stage. The diagnosis was reached within the first year of follow-up in 14 cases and after 1 year in seven (13 to 39 months). Fifteen of 21 cases of cancer were diagnosed in gastric ulcer patients. In conclusion, GED is an infrequent finding and its biologically neoplastic significance is confirmed by the results of the follow-up study: (1) in its mild form, it tends to regress but adequate subsequent check-ups are mandatory as it may associate with or evolve as cancer; (2) patients with moderate GED require strict follow-up since the lesion shows a higher cancer risk; (3) surgery is indicated for severe GED because gastric cancer develops in 75% of cases; and (4) patients with lesions indefinite for dysplasia should immediately undergo repeat endoscopy and biopsy. Such an approach allows gastric cancer to be detected at an early stage in a much higher percentage of cases than may be expected.
I.F. 3.12
- …
