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H pylori may trigger cancers by switching off a tumour suppressor
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Silencing of a cell surface adhesin in gastric mucosa in Helicobacter pylori infection may lead to gastric cancer, a molecular study has suggested. Methylation of the E-cadherin gene promoter—which inactivates its normal tumour suppressor function—was evident in gastric mucosa and significantly associated with H pylori infection in patients with chronic gastritis. It was absent from normal gastric mucosa but evident in 57% (12/21) of intestinal metaplasias, 58% (15/26) of primary gastric cancers, and 65% (21/32) of metastatic lymph node cancers. Methylation was congruent for 92% (11/12) intestinal metaplasias and primary cancers and 85% (17/20) primary and secondary metastatic cancers from the same patients.
Weaker immunostaining for E-cadherin—indicating methylation—occurred in most (11/13) primary cancers tested and most (7/9) metastatic cancers Methylation was significantly linked to depth of tumour invasion and spread. It was not related to H pylori infection here, however. The authors propose that H pylori infection of gastric mucosa
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