{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T17:57:23Z","timestamp":1787507843155,"version":"build-2736575974"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2018,4,15]],"date-time":"2018-04-15T00:00:00Z","timestamp":1523750400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["U1604174"],"award-info":[{"award-number":["U1604174"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Our previous works have demonstrated that\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      (\n                      <jats:italic>Hp<\/jats:italic>\n                      ) infection can alter histone H3 serine 10 phosphorylation status in gastric epithelial cells. However, whether\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010induced histone H3 serine 10 phosphorylation participates in gastric carcinogenesis is unknown. We investigate the expression of histone H3 serine 10 phosphorylation in various stages of gastric disease and explore its clinical implication.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      Stomach biopsy samples from 129 patients were collected and stained with histone H3 serine 10 phosphorylation, Ki67, and\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      by immunohistochemistry staining, expressed as labeling index. They were categorized into nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia, low\u2010grade intraepithelial neoplasia, high\u2010grade intraepithelial neoplasia, and intestinal\u2010type gastric cancer groups.\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      infection was determined by either\n                      <jats:sup>13<\/jats:sup>\n                      C\u2010urea breath test or immunohistochemistry staining.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010negative patients, labeling index of histone H3 serine 10 phosphorylation was gradually increased in nonatrophic gastritis, chronic atrophic gastritis, intestinal metaplasia groups, peaked at low\u2010grade intraepithelial neoplasia, and declined in high\u2010grade intraepithelial neoplasia and gastric cancer groups. In\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010infected patients, labeling index of histone H3 serine 10 phosphorylation followed the similar pattern as above, with increased expression over the corresponding\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010negative controls except in nonatrophic gastritis patient whose labeling index was decreased when compared with\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010negative control. Labeling index of Ki67 in\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010negative groups was higher in gastric cancer than chronic atrophic gastritis and low\u2010grade intraepithelial neoplasia groups, and higher in intestinal metaplasia group compared with chronic atrophic gastritis group. In\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010positive groups, Ki67 labeling index was increased stepwise from nonatrophic gastritis to gastric cancer except slightly decrease in chronic atrophic gastritis group. In addition, we noted that histone H3 serine 10 phosphorylation staining is accompanied with its location changes from gastric gland bottom expanded to whole gland as disease stage progress.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These results indicate that stepwise gastric carcinogenesis is associated with altered histone H3 serine 10 phosphorylation,\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      infection enhances histone H3 serine 10 phosphorylation expression in these processes; it is also accompanied with histone H3 serine 10 phosphorylation location change from gland bottom staining expand to whole gland expression. The results suggest that epigenetic dysregulation may play important roles in\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      \u2010induced gastric cancer.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/hel.12486","type":"journal-article","created":{"date-parts":[[2018,4,15]],"date-time":"2018-04-15T14:23:51Z","timestamp":1523802231000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["<i>Helicobacter pylori<\/i>\n                    infection\u2010induced H3Ser10 phosphorylation in stepwise gastric carcinogenesis and its clinical implications"],"prefix":"10.1111","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3066-1849","authenticated-orcid":false,"given":"Tao\u2010Tao","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Gastroenterology and Hepatology People's Hospital of Zhengzhou University  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