Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20994
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dc.contributor.authorAnagnostopoulos, G. K.en
dc.contributor.authorStefanou, D.en
dc.contributor.authorArkoumani, E.en
dc.contributor.authorKaragiannis, J.en
dc.contributor.authorParaskeva, K.en
dc.contributor.authorChalkley, L.en
dc.contributor.authorHabilomati, E.en
dc.contributor.authorTsianos, E.en
dc.contributor.authorAgnantis, N. J.en
dc.date.accessioned2015-11-24T19:11:59Z-
dc.date.available2015-11-24T19:11:59Z-
dc.identifier.issn1440-1746-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20994-
dc.rightsDefault Licence-
dc.subjectAdulten
dc.subjectAgeden
dc.subjectAged, 80 and overen
dc.subjectCell Cycle Proteins/*biosynthesisen
dc.subjectCyclin D1/*biosynthesisen
dc.subjectCyclin D3en
dc.subjectCyclin-Dependent Kinase Inhibitor p27/*biosynthesisen
dc.subjectCyclins/*biosynthesisen
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectImmunohistochemistryen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectPrecancerous Conditions/*metabolismen
dc.subjectStomach Neoplasms/*metabolismen
dc.subjectTumor Suppressor Protein p53/*biosynthesisen
dc.titleImmunohistochemical expression of cell-cycle proteins in gastric precancerous lesionsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1111/j.1440-1746.2007.05219.x-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/18397488-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1111/j.1440-1746.2007.05219.x/asset/j.1440-1746.2007.05219.x.pdf?v=1&t=h0f1ft4d&s=cd31b1873be34dde6986ec5cb797bb56ce39f8a1-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2008-
heal.abstractBACKGROUND: The early indicator for the subject predisposed to gastric cancer is abnormal proliferation of gastric epithelial cells, such as atrophic gastritis (AG), intestinal metaplasia (IM), and dysplasia, which have been considered as precancerous lesions of gastric cancer. To determine whether p53 protein, cyclins D1, and D3, and p27(kip1) play a role in the carcinogenesis pathway of gastric cancer, we performed an immunohistochemical study of their expression in gastric precancerous lesions. METHODS: A total of 1 45 endoscopic gastric biopsy specimens of AG, IM, and gastric dysplasia were studied. These molecular markers were localized by immunohistochemistry. RESULTS: P53 was expressed in 15% of cases with gastric dysplasia and not in the pre-dysplastic stages of the gastric mucosa. All cases were concerning high-grade dysplasia. Cyclin D1 protein was almost undetectable in the precancerous lesions of gastric cancer. Cyclin D3 protein overexpression was seen in 10% of biopsies with IM, and 50% of biopsies with gastric dysplasia. High expression of p27(kip1) protein was demonstrated in all cases of chronic gastritis. As atrophy, IM, and dysplasia develop, expression of p27(kip1) protein is suppressed. In total, 15% of dysplastic cases showed no expression of p27(kip1) protein. CONCLUSIONS: (i) P53 mutation must be a late event during the development of gastric cancer. (ii) Cyclin D1 protein overexpression may not play a role in the progression from normal to neoplastic gastric mucosa, while overexpression of cyclin D3 is an earlier event during gastric carcinogenesis, and its role must be further evaluated. (iii) Reduced expression of p27(kip1) is a rather early event in gastric tumorigenesis, before dysplastic changes occur.en
heal.journalNameJ Gastroenterol Hepatolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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