Cancer · 1998
Increased cell proliferation of the gastric mucosa in first-degree relatives of gastric carcinoma patients.
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Meining A, Hackelsberger A, Daenecke C, Stolte M, Bayerdörffer E, Ochsenkühn T
Аннотация
BACKGROUND: Studies not considering Helicobacter pylori infection have suggested the presence of a hereditary risk for gastric carcinoma. However, other studies have identified intrafamilial clustering of H. pylori infection as a causal factor in gastric carcinogenesis. This prompted the authors to study the effect of H. pylori and hereditary factors 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 carcinoma and 20 dyspeptic controls), 2 biopsy specimens each from the antrum and corpus were examined histologically. In addition, crude nuclei fractions were prepared from other biopsy specimens obtained in the same 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 G2/M-phases) was calculated.
RESULTS: In comparison with control patients, first-degree relatives of gastric carcinoma patients had increased mucosal proliferation of the antrum (Student's t test, P = 0.017). After excluding patients with H. pylori infection (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 increase the risk for developing gastric carcinoma via mucosal hyperproliferation, irrespective of H. pylori infection.
METHODS: In a total of 39 patients (19 first-degree relatives of patients with gastric carcinoma and 20 dyspeptic controls), 2 biopsy specimens each from the antrum and corpus were examined histologically. In addition, crude nuclei fractions were prepared from other biopsy specimens obtained in the same 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 G2/M-phases) was calculated.
RESULTS: In comparison with control patients, first-degree relatives of gastric carcinoma patients had increased mucosal proliferation of the antrum (Student's t test, P = 0.017). After excluding patients with H. pylori infection (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 increase the risk for developing gastric carcinoma via mucosal hyperproliferation, irrespective of H. pylori infection.