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dc.contributor.authorGarcía Solano, José
dc.contributor.authorTurpín, María del Carmen 
dc.contributor.authorTorres Moreno, Daniel
dc.contributor.authorHuertas López, Francisco
dc.contributor.authorTuomisto, Anne
dc.contributor.authorMäkinen, Markus J.
dc.contributor.authorConesa, Ana
dc.contributor.authorConesa Zamora, Pablo
dc.date.accessioned2018-11-20T12:44:08Z
dc.date.available2018-11-20T12:44:08Z
dc.date.issued2018
dc.identifier.issn1868-7083spa
dc.identifier.urihttp://hdl.handle.net/10641/1531
dc.description.abstractBackground: Altered methylation patterns are driving forces in colorectal carcinogenesis. The serrated adenocarcinoma (SAC) and sporadic colorectal carcinoma showing histological and molecular features of microsatellite instability (hmMSIH) are two endpoints of the so-called serrated pathological route sharing some characteristics but displaying a totally different immune response and clinical outcome. However, there are no studies comparing the methylome of these two subtypes of colorectal carcinomas. The methylation status of 450,000 CpG sites using the Infinium Human Methylation 450 BeadChip array was investigated in 48 colorectal specimens, including 39 SACs and 9 matched hmMSI-H. Results: Microarray data comparing SAC and hmMSI-H showed an enrichment in functions related to morphogenesis, neurogenesis, cytoskeleton, metabolism, vesicle transport and immune response and also significant differential methylation of 1540 genes, including CD14 and HLA-DOA which were more methylated in hmMSI-H than in SAC and subsequently validated at the CpG, mRNA and protein level using pyrosequencing, quantitative polymerase chain reaction (qPCR) and immunohistochemistry. Conclusions: These results demonstrate particular epigenetic regulation patterns in SAC which may help to define key molecules responsible for the characteristic weak immune response of SAC and identify potential targets for treating SAC, which lacks molecular targeted therapy.spa
dc.language.isoengspa
dc.publisherClinical Epigeneticsspa
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.subjectColorectal cancerspa
dc.subjectMethylomespa
dc.subjectImmune responsespa
dc.subjectMicrosatellite instabilityspa
dc.subjectEpigeneticsspa
dc.subjectColon carcinogenesisspa
dc.titleTwo histologically colorectal carcinomas subsets from the serrated pathway show different methylome signatures and diagnostic biomarkers.spa
dc.typearticlespa
dc.description.versionpost-printspa
dc.rights.accessRightsopenAccessspa
dc.description.extent4929 KBspa
dc.identifier.doi10.1186/s13148-018-0571-3spa


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Atribución-NoComercial-SinDerivadas 3.0 España
Except where otherwise noted, this item's license is described as Atribución-NoComercial-SinDerivadas 3.0 España