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Deregulation of E‐cadherin–catenin complex in precancerous lesions of gastric adenocarcinoma
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AbstractBackground and Aim: Decrease in expression of the E‐cadherin–catenin complex is an important element in gastric carcinogenesis. However, the expression of the complex in gastric precancerous lesions has not been well studied. The present study aimed to examine the serial change in expression of E‐cadherin–catenin complex in the precancerous lesions of gastric cancer patients.Methods: Gastrectomy specimens of 40 patients with gastric cancer were retrieved. Areas with chronic gastritis, atrophic gastritis, intestinal metaplasia and adenocarcinoma were identified and immunostained for α‐catenin, β‐catenin and E‐cadherin. The results were scored semiquantitatively by two independent pathologists using a validated scoring system.Results: A significant decrease in score was observed in 5% (1/22) of α‐catenin, 0% (0/22) of β‐catenin and 9% (2/22) of E‐cadherin in chronic atrophic gastritis patients, and in 28% (5/18) of α‐catenin, 67% (10/15) of β‐catenin and 57% (8/14) of E‐cadherin in intestinal metaplasia patients. The scoring of α‐catenin, β‐catenin and E‐cadherin correlated with each other. Forty‐three percent of patients had concordant changes of scores along the gastritis–adenocarcinoma sequence. There was no association between Helicobacter pylori status and E‐cadherin–catenin complex expression.Conclusion: Deregulation of the E‐cadherin–catenin complex was observed in the majority of precancerous lesions in patients with gastric adenocarcinoma, which has potential diagnostic and therapeutic implications.© 2003 Blackwell Publishing Asia Pty Ltd
Title: Deregulation of E‐cadherin–catenin complex in precancerous lesions of gastric adenocarcinoma
Description:
AbstractBackground and Aim: Decrease in expression of the E‐cadherin–catenin complex is an important element in gastric carcinogenesis.
However, the expression of the complex in gastric precancerous lesions has not been well studied.
The present study aimed to examine the serial change in expression of E‐cadherin–catenin complex in the precancerous lesions of gastric cancer patients.
Methods: Gastrectomy specimens of 40 patients with gastric cancer were retrieved.
Areas with chronic gastritis, atrophic gastritis, intestinal metaplasia and adenocarcinoma were identified and immunostained for α‐catenin, β‐catenin and E‐cadherin.
The results were scored semiquantitatively by two independent pathologists using a validated scoring system.
Results: A significant decrease in score was observed in 5% (1/22) of α‐catenin, 0% (0/22) of β‐catenin and 9% (2/22) of E‐cadherin in chronic atrophic gastritis patients, and in 28% (5/18) of α‐catenin, 67% (10/15) of β‐catenin and 57% (8/14) of E‐cadherin in intestinal metaplasia patients.
The scoring of α‐catenin, β‐catenin and E‐cadherin correlated with each other.
Forty‐three percent of patients had concordant changes of scores along the gastritis–adenocarcinoma sequence.
There was no association between Helicobacter pylori status and E‐cadherin–catenin complex expression.
Conclusion: Deregulation of the E‐cadherin–catenin complex was observed in the majority of precancerous lesions in patients with gastric adenocarcinoma, which has potential diagnostic and therapeutic implications.
© 2003 Blackwell Publishing Asia Pty Ltd.
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