Do gene expressions differ between gastritis with and without helicobacter pylori?

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dc.authorid0000-0002-0901-9192en_US
dc.authorid0000-0003-4096-4261
dc.authorid0000-0001-7965-6229
dc.contributor.authorBoran, Çetin
dc.contributor.authorBalaban, Hatice Yasemin
dc.contributor.authorYılmaz, Fahri
dc.date.accessioned2021-06-23T19:26:40Z
dc.date.available2021-06-23T19:26:40Z
dc.date.issued2010
dc.departmentBAİBÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.description.abstractObjective: Helicobacter pylori infection is a well-defined risk factor for the development of gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. However, mechanisms of carcinogenesis in Helicobacter gastritis need to be elucidated. We aimed in this study to determine the immunohistochemical expressions of some cancer-associated genes, and to show differences between Helicobacter gastritis and Helicobacter-negative gastritis. Material and Methods: Sixty-three endoscopic biopsy samples were selected. The samples comprised of normal gastric mucosa (20 samples), Helicobacter gastritis (22 samples), and Helicobacter-negative gastritis (21 samples). Paraffin sections of samples were processed immunohistochemically with some suppressor genes (Rb, p53), protooncogenes (EGFR, cyclin D1), and a heat shock protein, HSP 105. The gene expressions in both crypt epithelia and lymphoid infiltrate were evaluated separately. Results: In epithelia; expressions of cyclin DI, p53, HSP 105, and EGFR were higher in Helicobacter-negative gastritis than in Helicobacter gastritis (p< 0.0001). Immune expression of HSP 105 in Helicobacter gastritis was lower than in control group (p= 0.008) as well as in Helicobacter-negative gastritis. However, expression of Rb was higher in Helicobacter gastritis than in Helicobacter-negative gastritis (p= 0.034). In lymphoid infiltrate; immune reactions for p53 and cyclin D1 were negative in all samples. Expressions of Rb, EGFR, and HSP 105 in lymphoid infiltrate were similar to expressions in epithelia for all groups. Conclusion: We can suggest that development of gastric cancer has a different pathway in Helicobacter gastritis when compared to the one Helicobacter-negative gastritis. In addition, decrease of heat shock proteins in Helicobacter gastritis may lead to sensitivity of crypt epithelia and lymphoid infiltrate for carcinogenic mutations.en_US
dc.identifier.doi10.5336/medsci.2009-14585
dc.identifier.endpage1813en_US
dc.identifier.issn1300-0292
dc.identifier.issue6en_US
dc.identifier.scopus2-s2.0-78650929760en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage1806en_US
dc.identifier.urihttps://doi.org/10.5336/medsci.2009-14585
dc.identifier.urihttps://hdl.handle.net/20.500.12491/6618
dc.identifier.volume30en_US
dc.identifier.wosWOS:000287053500004en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorBoran, Çetin
dc.institutionauthorBalaban, Hatice Yasemin
dc.institutionauthorYılmaz, Fahri
dc.language.isoenen_US
dc.publisherOrtadogu Ad Pres & Publ Coen_US
dc.relation.ispartofTurkiye Klinikleri Tip Bilimleri Dergisien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCocarcinogenesisen_US
dc.subjectCyclin D1en_US
dc.subjectGenes, p53en_US
dc.subjectEGFR Proteinen_US
dc.titleDo gene expressions differ between gastritis with and without helicobacter pylori?en_US
dc.typeArticleen_US

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