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dc.contributor.author Patai, Árpád V
dc.contributor.author Valcz, Gábor
dc.contributor.author Hollósi, Péter
dc.contributor.author Kalmár, Alexandra
dc.contributor.author Péterfia, Bálint
dc.contributor.author Patai, Árpád
dc.contributor.author Wichmann, Barnabás
dc.contributor.author Spisak S
dc.contributor.author Barták, Barbara Kinga
dc.contributor.author Leiszter, Katalin
dc.contributor.author Tóth, Kinga
dc.contributor.author Sipos, Ferenc
dc.contributor.author Kovalszky, Ilona
dc.contributor.author Péter, Zoltán
dc.contributor.author Miheller, Pál
dc.contributor.author Tulassay, Zsolt
dc.contributor.author Molnár, Béla
dc.date.accessioned 2018-09-14T06:38:10Z
dc.date.available 2018-09-14T06:38:10Z
dc.date.issued 2015
dc.identifier 84942897786
dc.identifier.citation pagination=e0133836, pages: 19; journalVolume=10; journalIssueNumber=8; journalTitle=PLOS ONE;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/5980
dc.identifier.uri doi:10.1371/journal.pone.0133836
dc.description.abstract Microarray analysis of promoter hypermethylation provides insight into the role and extent of DNA methylation in the development of colorectal cancer (CRC) and may be co-monitored with the appearance of driver mutations. Colonic biopsy samples were obtained endoscopically from 10 normal, 23 adenoma (17 low-grade (LGD) and 6 high-grade dysplasia (HGD)), and 8 ulcerative colitis (UC) patients (4 active and 4 inactive). CRC samples were obtained from 24 patients (17 primary, 7 metastatic (MCRC)), 7 of them with synchronous LGD. Field effects were analyzed in tissues 1 cm (n = 5) and 10 cm (n = 5) from the margin of CRC. Tissue materials were studied for DNA methylation status using a 96 gene panel and for KRAS and BRAF mutations. Expression levels were assayed using whole genomic mRNA arrays. SFRP1 was further examined by immunohistochemistry. HT29 cells were treated with 5-aza-2' deoxycytidine to analyze the reversal possibility of DNA methylation. More than 85% of tumor samples showed hypermethylation in 10 genes (SFRP1, SST, BNC1, MAL, SLIT2, SFRP2, SLIT3, ALDH1A3, TMEFF2, WIF1), whereas the frequency of examined mutations were below 25%. These genes distinguished precancerous and cancerous lesions from inflamed and healthy tissue. The mRNA alterations that might be caused by systematic methylation could be partly reversed by demethylation treatment. Systematic changes in methylation patterns were observed early in CRC carcinogenesis, occuring in precursor lesions and CRC. Thus we conclude that DNA hypermethylation is an early and systematic event in colorectal carcinogenesis, and it could be potentially reversed by systematic demethylation therapy, but it would need more in vitro and in vivo experiments to support this theory.
dc.relation.ispartof urn:issn:1932-6203
dc.title Comprehensive DNA Methylation Analysis Reveals a Common Ten-Gene Methylation Signature in Colorectal Adenomas and Carcinomas
dc.type Journal Article
dc.date.updated 2018-07-20T07:20:07Z
dc.language.rfc3066 en
dc.identifier.mtmt 2934722
dc.identifier.wos 000359919900003
dc.identifier.pubmed 26291085
dc.contributor.department SE/AOK/K/II. Sz. Belgyógyászati Klinika
dc.contributor.department SE/AOK/I/I. Sz. Patológiai és Kísérleti Rákkutató Intézet
dc.contributor.institution Semmelweis Egyetem


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