Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/47271
Campo DC Valoridioma
dc.contributor.authorAlonso, Sergioen_US
dc.contributor.authorDai, Yuichien_US
dc.contributor.authorYamashita, Kentaroen_US
dc.contributor.authorHoriuchi, Shinaen_US
dc.contributor.authorDai, Tomokoen_US
dc.contributor.authorMatsunaga, Akihiroen_US
dc.contributor.authorSánchez-Muñoz, Rosaen_US
dc.contributor.authorBilbao-Sieyro, Cristinaen_US
dc.contributor.authorDaz-Chico, Juan Carlosen_US
dc.contributor.authorChernov, Andrei V.en_US
dc.contributor.authorStrongin, Alex Y.en_US
dc.contributor.authorPerucho, Manuelen_US
dc.contributor.otherAlonso, Sergio-
dc.contributor.otherBILBAO SIEYRO, CRISTINA-
dc.contributor.otherDiaz-Chico, Juan-
dc.contributor.otherStrongin, Alex-
dc.date.accessioned2018-11-23T12:12:39Z-
dc.date.available2018-11-23T12:12:39Z-
dc.date.issued2015en_US
dc.identifier.issn1949-2553en_US
dc.identifier.urihttp://hdl.handle.net/10553/47271-
dc.description.abstractSomatic hypermethylation of the O-6-methylguanine-DNA methyltransferase gene (MGMT) was previously associated with G > A transition mutations in KRAS and TP53 in colorectal cancer (CRC). We tested the association of MGMT methylation with G > A mutations in KRAS and TP53 in 261 CRCs. Sixteen cases, with and without MGMT hypermethylation, were further analyzed by exome sequencing. No significant association of MGMT methylation with G > A mutations in KRAS, TP53 or in the whole exome was found (p > 0.5 in all comparisons). The result was validated by in silico comparison with 302 CRCs from The Cancer Genome Atlas (TCGA) consortium dataset. Transcriptional silencing associated with hypermethylation and stratified into monoallelic and biallelic. We also found a significant clustering (p = 0.001) of aberrant hypermethylation of MGMT and the matrix metalloproteinase gene ADAMTS14 in normal colonic mucosa of CRC patients. This suggested the existence of an epigenetic field defect for cancerization disrupting the methylation patterns of several loci, including MGMT or ADAMTS14, that may lead to predictive biomarkers for CRC. Methylation of these loci in normal mucosa was more frequent in elder (p = 0.001) patients, and particularly in African Americans (p = 1 x 10(-5)), thus providing a possible mechanistic link between somatic epigenetic alterations and CRC racial disparities in North America.en_US
dc.languageengen_US
dc.relation.ispartofOncotargeten_US
dc.sourceOncotarget[ISSN 1949-2553],v. 6 (5), p. 3420-3431en_US
dc.subject32 Ciencias médicasen_US
dc.subject320101 Oncologíaen_US
dc.subject.otherCpg Island Hypermethylationen_US
dc.subject.otherGene O-6-Methylguanine-Dna Methyltransferaseen_US
dc.subject.otherDna Mismatch Repairen_US
dc.subject.otherColorectal-Canceren_US
dc.subject.otherPromoter Hypermethylationen_US
dc.subject.otherRas Oncogenesen_US
dc.subject.otherK-Rasen_US
dc.subject.otherMutator Phenotypeen_US
dc.subject.otherG-Cen_US
dc.subject.otherMutationsen_US
dc.titleMethylation of MGMT and ADAMTS14 in normal colon mucosa: Biomarkers of a field defect for cancerization preferentially targeting elder African-Americansen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.18632/oncotarget.2852en_US
dc.identifier.scopus84923311865-
dc.identifier.isi000352694400065-
dcterms.isPartOfOncotarget
dcterms.sourceOncotarget[ISSN 1949-2553],v. 6 (5), p. 3420-3431
dc.contributor.authorscopusid12771069700-
dc.contributor.authorscopusid57202127267-
dc.contributor.authorscopusid35462905700-
dc.contributor.authorscopusid7202162198-
dc.contributor.authorscopusid57200714689-
dc.contributor.authorscopusid56514814100-
dc.contributor.authorscopusid36093322500-
dc.contributor.authorscopusid56294291600-
dc.contributor.authorscopusid6701492347-
dc.contributor.authorscopusid24474211000-
dc.contributor.authorscopusid35518794900-
dc.contributor.authorscopusid7006337861-
dc.description.lastpage3431en_US
dc.description.firstpage3420en_US
dc.relation.volume6en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.identifier.wosWOS:000352694400065-
dc.contributor.daisngid964210-
dc.contributor.daisngid5456847-
dc.contributor.daisngid542776-
dc.contributor.daisngid12375109-
dc.contributor.daisngid4808341-
dc.contributor.daisngid1731381-
dc.contributor.daisngid6587931-
dc.contributor.daisngid2205075-
dc.contributor.daisngid749099-
dc.contributor.daisngid14172339-
dc.contributor.daisngid1188679-
dc.contributor.daisngid90098-
dc.contributor.daisngid348212-
dc.identifier.investigatorRIDG-5145-2011-
dc.identifier.investigatorRIDR-6779-2018-
dc.identifier.investigatorRIDH-1527-2015-
dc.identifier.investigatorRIDNo ID-
dc.description.numberofpages12en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Alonso, S-
dc.contributor.wosstandardWOS:Dai, YC-
dc.contributor.wosstandardWOS:Yamashita, K-
dc.contributor.wosstandardWOS:Horiuchi, S-
dc.contributor.wosstandardWOS:Dai, T-
dc.contributor.wosstandardWOS:Matsunaga, A-
dc.contributor.wosstandardWOS:Sanchez-Munoz, R-
dc.contributor.wosstandardWOS:Bilbao-Sieyro, C-
dc.contributor.wosstandardWOS:Daz-Chico, JC-
dc.contributor.wosstandardWOS:Chernov, AV-
dc.contributor.wosstandardWOS:Strongin, AY-
dc.contributor.wosstandardWOS:Perucho, M-
dc.date.coverdateEnero 2015en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr2,262
dc.description.jcr5,008
dc.description.sjrqQ1
dc.description.jcrqQ1
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.author.deptDepartamento de Morfología-
crisitem.author.deptGIR IUIBS: Bioquímica-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Bioquímica y Biología Molecular, Fisiología, Genética e Inmunología-
crisitem.author.orcid0000-0002-4796-1445-
crisitem.author.orcid0000-0002-0944-990X-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameBilbao Sieyro, Cristina-
crisitem.author.fullNameDíaz Chico, Juan Carlos-
Colección:Artículos
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