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Mutations in Helicobacter pylori infected patients with chronic gastritis, intestinal type of gastric cancer and familial gastric cancer

cris.virtual.author-orcid0000-0002-0153-4317
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dc.abstract.enBackground Development of sequential changes of mucous leading to gastric cancer and familial cases of gastric cancer of intestinal type is widely connected with Helicobacter pylori infections. In this study we analysed variants of genes involved in cancerogenesis and inflammatory processes of intestines in patients infected with H.pylori. Our goal was to test whether mutations in these genes predestinate to development of gastric cancer, and whether there is a genetic factor that makes it more likely for infections with H.pylori to cause gastric cancer. As infections with H. pylori are relatively common, discovering such genetic predispositions could be used for establishing risk-groups and for planning treatments. Methods Our studies cover analysis of variants in genes involved in cancerogenesis: TP53 (rs11540652, rs587782329, COSM10771), MSH2 (rs193922376), MLH1 (rs63750217), and inflammatory processes of intestine: NOD2 (rs2066847, rs2066842), IL1A (rs1800587) and IL1B (rs1143634) from H.pylori-infected patients. Results Mutations were more common in the group of patients with gastric cancer of intestinal type and familial cases of gastric cancer in comparison with patients with chronic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia or gastric cancer (p-value=0.00824), with the prevalence of p53 mutations in patients with familial gastric cancer vs. patients with other changes of mucosa (p-value=0.000049). Additionally, gastric cancer patients have mainly genotype TT or CT of the rs2066842 variant of the NOD2 gene. Conclusions The lack of statistically significant changes of other interleukin genes involved in inflammatory processes may suggest the presence of H.pylori infection as a potential trigger for the development of the inflammatory process of the mucosa, leading through microbiota dysbiosis to the development of enteric gastric cancer. Mutations in analysed genes correlated with more severe mucosal changes, with a much more frequent presence of TP53 gene mutations, with a limited presence of other mutations in the familial history of gastric cancer.
dc.affiliationWydział Rolnictwa, Ogrodnictwa i Bioinżynierii
dc.affiliation.instituteKatedra Biochemii i Biotechnologii
dc.contributor.authorHnatyszyn, Andrzej
dc.contributor.authorSzalata, Marlena
dc.contributor.authorZielińska, Aleksandra
dc.contributor.authorWielgus, Karolina
dc.contributor.authorDanielewski, Mikołaj
dc.contributor.authorHnatyszyn, Piotr Tomasz
dc.contributor.authorPławski, Andrzej
dc.contributor.authorWalkowiak, Jarosław
dc.contributor.authorSłomski, Ryszard
dc.date.access2024-08-29
dc.date.accessioned2024-08-29T10:17:04Z
dc.date.available2024-08-29T10:17:04Z
dc.date.copyright2024-06-12
dc.date.issued2024
dc.description.abstract<jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> <jats:p>Development of sequential changes of mucous leading to gastric cancer and familial cases of gastric cancer of intestinal type is widely connected with <jats:italic>Helicobacter pylori</jats:italic> infections. In this study we analysed variants of genes involved in cancerogenesis and inflammatory processes of intestines in patients infected with <jats:italic>H.pylori</jats:italic>. Our goal was to test whether mutations in these genes predestinate to development of gastric cancer, and whether there is a genetic factor that makes it more likely for infections with <jats:italic>H.pylori</jats:italic> to cause gastric cancer. As infections with <jats:italic>H. pylori</jats:italic> are relatively common, discovering such genetic predispositions could be used for establishing risk-groups and for planning treatments.</jats:p> </jats:sec><jats:sec> <jats:title>Methods</jats:title> <jats:p>Our studies cover analysis of variants in genes involved in cancerogenesis: <jats:italic>TP53</jats:italic> (rs11540652, rs587782329, COSM10771), <jats:italic>MSH2</jats:italic> (rs193922376), <jats:italic>MLH1</jats:italic> (rs63750217), and inflammatory processes of intestine: <jats:italic>NOD2</jats:italic> (rs2066847, rs2066842), <jats:italic>IL1A</jats:italic> (rs1800587) and <jats:italic>IL1B</jats:italic> (rs1143634) from <jats:italic>H.pylori-</jats:italic>infected patients.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>Mutations were more common in the group of patients with gastric cancer of intestinal type and familial cases of gastric cancer in comparison with patients with chronic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia or gastric cancer (p-value = 0.00824), with the prevalence of p53 mutations in patients with familial gastric cancer vs. patients with other changes of mucosa (p-value = 0.000049). Additionally, gastric cancer patients have mainly genotype TT or CT of the rs2066842 variant of the <jats:italic>NOD2</jats:italic> gene.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusions</jats:title> <jats:p>The lack of statistically significant changes of other interleukin genes involved in inflammatory processes may suggest the presence of <jats:italic>H.pylori</jats:italic> infection as a potential trigger for the development of the inflammatory process of the mucosa, leading through microbiota dysbiosis to the development of enteric gastric cancer. Mutations in analysed genes correlated with more severe mucosal changes, with a much more frequent presence of <jats:italic>TP53</jats:italic> gene mutations, with a limited presence of other mutations in the familial history of gastric cancer.</jats:p> </jats:sec>
dc.description.accesstimeat_publication
dc.description.bibliographybibliogr.
dc.description.financepublication_nocost
dc.description.financecost0,00
dc.description.if2,0
dc.description.points70
dc.description.reviewreview
dc.description.versionfinal_published
dc.description.volume22
dc.identifier.doi10.1186/s13053-024-00282-8
dc.identifier.eissn1897-4287
dc.identifier.issn1731-2302
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/1703
dc.identifier.weblinkhttps://hccpjournal.biomedcentral.com/articles/10.1186/s13053-024-00282-8
dc.languageen
dc.relation.ispartofHereditary Cancer in Clinical Practice
dc.relation.pagesart. 9
dc.rightsCC-BY
dc.sciencecloudnosend
dc.share.typeOPEN_JOURNAL
dc.subject.enHelicobacter pylori
dc.subject.enChronic gastritis
dc.subject.enIntestinal type of gastric cancer
dc.subject.enFamilial gastric cancer
dc.subject.enDNA variants
dc.subject.enMolecular diagnostics
dc.subject.enTP53
dc.subject.enNOD2
dc.titleMutations in Helicobacter pylori infected patients with chronic gastritis, intestinal type of gastric cancer and familial gastric cancer
dc.typeJournalArticle
dspace.entity.typePublication
oaire.citation.issue1
oaire.citation.volume22
project.funder.nameInstytut Genetyki Człowieka PAN/ Uniwersytet Przyrodniczy w Poznaniu/ Fundacja na rzecz Rozwoju Biotechnologii i Genetyki POLBIOGEN