{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:38:23Z","timestamp":1787017103810,"version":"build-2736575974"},"reference-count":33,"publisher":"BMJ","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Clin Pathol"],"accepted":{"date-parts":[[2011,4,18]]},"published-print":{"date-parts":[[2011,8]]},"abstract":"<jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>\n                      Cancer, particularly gastric cancer (GC), is prevalently an epigenetic phenomenon that is dependent on an altered DNA methylation pattern. In gastric carcinogenesis, many genes show aberrant methylation; however, none of them may be used as a biomarker of cancer risk and progression. The authors aimed to evaluate the global DNA methylation of gastric mucosa in\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      (\n                      <jats:italic>Hp<\/jats:italic>\n                      )-related chronic gastritis, in GC and in 10 patients with preneoplastic lesions (ie, atrophy and intestinal metaplasia) followed up for 10\u2005years.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The authors analysed 93 dyspeptic patients who underwent upper endoscopy, 41 surgical GC samples and 10 patients with preneoplastic gastric lesions followed up for 10\u2005years after successful\n                      <jats:italic>Hp<\/jats:italic>\n                      eradication therapy. Global DNA methylation status and surrogate markers of cell proliferation and apoptosis were evaluated by immunohistochemistry using the anti-5-methylcytosine (5-MC), anti-Ki-67 and anti-p53 (anti-apoptotic marker)-specific antibodies, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Global DNA methylation of gastric mucosa gradually decreased from normal mucosa to\n                      <jats:italic>Hp<\/jats:italic>\n                      -positive gastritis,\n                      <jats:italic>Hp<\/jats:italic>\n                      -positive chronic atrophic gastritis, independent of Cag-A status and GC; however, the variation was significant (p&lt;0.05) only between\n                      <jats:italic>Hp<\/jats:italic>\n                      -negative subjects and\n                      <jats:italic>Hp<\/jats:italic>\n                      -positive chronic gastritis. Interestingly, the 5-MC immunostaining was absent in areas of intestinal metaplasia. In the 10 patients with preneoplastic lesions, global DNA methylation decreased over time despite the eradication of\n                      <jats:italic>Hp<\/jats:italic>\n                      infection, but reached significance only at 10\u2005years versus baseline. The 5-MC immunostaining negatively correlated with Ki-67 and p53 expression in all groups.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Global DNA hypomethylation is an early molecular event in\n                      <jats:italic>Hp<\/jats:italic>\n                      -related gastric carcinogenesis. Further studies with more cases and a longer follow-up are needed to establish the potential GC predictive role of DNA hypomethylation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jcp.2010.087858","type":"journal-article","created":{"date-parts":[[2011,5,27]],"date-time":"2011-05-27T00:30:09Z","timestamp":1306456209000},"page":"677-682","source":"Crossref","is-referenced-by-count":44,"title":["Global DNA hypomethylation is an early event in\n                    <i>Helicobacter pylori<\/i>\n                    -related gastric 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