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dc.contributor.authorMäki-Nevala, Satu
dc.contributor.authorUkwattage, Sanjeevi
dc.contributor.authorWirta, Erkki-Ville
dc.contributor.authorAhtiainen, Maarit
dc.contributor.authorRistimäki, Ari
dc.contributor.authorSeppälä, Toni T.
dc.contributor.authorLepistö, Anna
dc.contributor.authorMecklin, Jukka-Pekka
dc.contributor.authorPeltomäki, Päivi
dc.date.accessioned2021-10-05T08:35:38Z
dc.date.available2021-10-05T08:35:38Z
dc.date.issued2021
dc.identifier.citationMäki-Nevala, S., Ukwattage, S., Wirta, E.-V., Ahtiainen, M., Ristimäki, A., Seppälä, T. T., Lepistö, A., Mecklin, J.-P., & Peltomäki, P. (2021). Immunoprofiles and DNA Methylation of Inflammatory Marker Genes in Ulcerative Colitis-Associated Colorectal Tumorigenesis. <i>Biomolecules</i>, <i>11</i>(10), Article 1440. <a href="https://doi.org/10.3390/biom11101440" target="_blank">https://doi.org/10.3390/biom11101440</a>
dc.identifier.otherCONVID_101329330
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/78023
dc.description.abstractImmunological and epigenetic changes are interconnected and contribute to tumorigenesis. We determined the immunoprofiles and promoter methylation of inflammation-related genes for colitis-associated colorectal carcinomas (CA-CRC). The results were compared with Lynch syndrome (LS)-associated colorectal tumors, which are characterized by an active immune environment through inherited mismatch repair defects. CA-CRCs (n = 31) were immunohistochemically evaluated for immune cell scores (ICSs) and PDCD1 and CD274 expression. Seven inflammation-associated genes (CD274, NTSR1, PPARG, PTGS2, PYCARD, SOCS1, and SOCS2), the repair gene MGMT, and eight standard marker genes for the CpG Island Methylator Phenotype (CIMP) were investigated for promoter methylation in CA-CRCs, LS tumors (n = 29), and paired normal mucosae by multiplex ligation-dependent probe amplification. All but one CA-CRCs were microsatellite-stable and all LS tumors were microsatellite-unstable. Most CA-CRCs had a high ICS (55%) and a positive CD274 expression in immune cells (52%). NTSR1 revealed frequent tumor-specific hypermethylation in CA-CRC and LS. When compared to LS mucosae, normal mucosae from patients with CA-CRC showed significantly higher methylation of NTSR1 and most CIMP markers. In conclusion, CA-CRCs share a frequent ICShigh/CD274pos expression pattern with LS tumors. Elevated methylation in normal mucosa may indicate field cancerization as a feature of CA-CRC-associated tumorigenesis.en
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherMDPI AG
dc.relation.ispartofseriesBiomolecules
dc.rightsCC BY 4.0
dc.subject.otherLynch syndrome
dc.subject.otherulcerative colitis
dc.subject.othercolon cancer
dc.subject.otherimmune cell score
dc.subject.otherDNA methylation
dc.subject.otherinflammation-associated genes
dc.titleImmunoprofiles and DNA Methylation of Inflammatory Marker Genes in Ulcerative Colitis-Associated Colorectal Tumorigenesis
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-202110055075
dc.contributor.laitosLiikuntatieteellinen tiedekuntafi
dc.contributor.laitosFaculty of Sport and Health Sciencesen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.description.reviewstatuspeerReviewed
dc.relation.issn2218-273X
dc.relation.numberinseries10
dc.relation.volume11
dc.type.versionpublishedVersion
dc.rights.copyright© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
dc.rights.accesslevelopenAccessfi
dc.subject.ysohaavainen koliitti
dc.subject.ysoLynchin oireyhtymä
dc.subject.ysoimmuunivaste
dc.subject.ysoepigenetiikka
dc.subject.ysoDNA-metylaatio
dc.subject.ysotulehdus
dc.subject.ysosuolistosyövät
dc.subject.ysopaksusuolisyöpä
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p22574
jyx.subject.urihttp://www.yso.fi/onto/yso/p23697
jyx.subject.urihttp://www.yso.fi/onto/yso/p21599
jyx.subject.urihttp://www.yso.fi/onto/yso/p24631
jyx.subject.urihttp://www.yso.fi/onto/yso/p38350
jyx.subject.urihttp://www.yso.fi/onto/yso/p1049
jyx.subject.urihttp://www.yso.fi/onto/yso/p25845
jyx.subject.urihttp://www.yso.fi/onto/yso/p5937
dc.rights.urlhttps://creativecommons.org/licenses/by/4.0/
dc.relation.doi10.3390/biom11101440
jyx.fundinginformationThis study was funded by Jane and Aatos Erkko Foundation (to P.P., J.‐P.M. and T.T.S.); the Academy of Finland (grant numbers 330606 to P.P. and 331284 to S.M.‐N.); the Finnish Cancer Foundation (to P.P., J.‐P.M., T.T.S. and A.R.); Finnish Medical Foundation (to T.T.S.); Emil Aaltonen Foundation (to T.T.S.); the Sigrid Juselius Foundation (to P.P., T.T.S. and A.R.) and the HiLIFE Fel‐ lows 2017–2020 (to P.P.).


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