INCREASED CELL-PROLIFERATION OF THE GASTRIC-MUCOSA IN FIRST-DEGREE RELATIVES OF GASTRIC-CARCINOMA PATIENTS

Citation
A. Meining et al., INCREASED CELL-PROLIFERATION OF THE GASTRIC-MUCOSA IN FIRST-DEGREE RELATIVES OF GASTRIC-CARCINOMA PATIENTS, Cancer, 83(5), 1998, pp. 876-881
Citations number
23
Categorie Soggetti
Oncology
Journal title
CancerACNP
ISSN journal
0008543X
Volume
83
Issue
5
Year of publication
1998
Pages
876 - 881
Database
ISI
SICI code
0008-543X(1998)83:5<876:ICOTGI>2.0.ZU;2-O
Abstract
BACKGROUND. Studies not considering Helicobacter pylori infection have suggested the presence of a hereditary risk for gastric carcinoma. Ho wever, other studies have identified intrafamilial clustering of H. py lori infection as a causal factor in gastric carcinogenesis. This prom pted the authors to study the effect of II. pylori and hereditary fact ors on the proliferation of gastric mucosa because hyperproliferation appears to be an early step in carcinogenesis. METHODS. In a total of 39 patients (19 first-degree relatives of patients with gastric carcin oma and 20 dyspeptic controls), 2 biopsy specimens each from the antru m and corpus were examined histologically. In addition, crude nuclei f ractions were prepared from other biopsy specimens obtained in the sam e manner. Nuclei were fixed in 70% ethanol and stained with propidium iodine prior to measurement. A cell cycle analysis was performed using a flow cytometer. For analysis a proliferative index (PI) (percentage of nuclei in the S- and G(2)/M-phases) was calculated. RESULTS. In co mparison with control patients, first-degree relatives of gastric carc inoma patients had increased mucosal proliferation of the antrum (Stud ent's t test, P = 0.017). After excluding patients with H. pylori infe ction (12 in each group), relatives of gastric carcinoma patients had significantly increased proliferation not only in the antrum (PI: 16.5 vs. 12.1; P = 0.043), but also in the corpus (PI: 17.2 vs. 13.0; P = 0.024). CONCLUSIONS. A family history of gastric carcinoma may increas e the risk for developing gastric carcinoma via mucosal hyperprolifera tion, irrespective of H. pylori infection. (C) 1998 American Cancer So ciety.