Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/143142
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dc.contributor.authorEstévez-García, Purificación-
dc.contributor.authorLópez-Calderero, Iker-
dc.contributor.authorMolina-Pinelo, Sonia-
dc.contributor.authorMuñoz-Galván, Sandra-
dc.contributor.authorSalinas, Ana-
dc.contributor.authorGómez Izquierdo, Lourdes-
dc.contributor.authorLucena-Cacace, Antonio-
dc.contributor.authorFelipe-Abrio, Blanca-
dc.contributor.authorPaz-Ares, Luis-
dc.contributor.authorGarcía-Carbonero, Rocío-
dc.contributor.authorCarnero, Amancio-
dc.date.accessioned2017-01-30T11:01:09Z-
dc.date.available2017-01-30T11:01:09Z-
dc.date.issued2013-07-
dc.identifierissn: 1078-0432-
dc.identifiere-issn: 1557-3265-
dc.identifier.citationClinical Cancer Research 19(14): 3925-3935 (2013)-
dc.identifier.urihttp://hdl.handle.net/10261/143142-
dc.description.abstract[Purpose+ The genomic region 17q21 is frequently associated with microsatellite instability and LOH in cancer, including gastric and colorectal carcinomas. This region contains several putative tumor suppressor genes, including Brca1, NM23, prohibitin, and spinophilin (Spn, PPP1R9B, neurabin II). The scaffold protein Spn is one of the regulatory subunits of phosphatase-1 (PP1) that targets PP1 to distinct subcellular locations and couples PP1 to its target. Thus, Spn may alter cell-cycle progression via the regulation of the phosphorylation status of the retinoblastoma protein, a direct target of PP1. Therefore, we analyzed whether Spn levels were reduced in colorectal carcinomas and whether Spn levels correlated with prognosis or response to therapy.-
dc.description.abstract[Experimental Design] By means of immunohistochemistry or quantitative PCR, we studied the levels of Spn in stages II, III, and IV colorectal carcinoma tumors and correlated to other clinicopathologic features as well as prognosis or response to therapy.-
dc.description.abstract[Results] Spn was lost in a percentage of human gastric, small intestine, and colorectal carcinomas. In patients with colorectal carcinoma, tumoral Spn downregulation correlated with a more aggressive histologic phenotype (poorer tumor differentiation and higher proliferative Ki67 index). Consistent with this observation, lower Spn protein expression levels were associated with faster relapse and poorer survival in patients with stage III colorectal carcinoma, particularly among those receiving adjuvant fluoropyrimidine therapy. We validated this result in an independent cohort of patients with metastatic colorectal carcinoma treated with standard chemotherapy. Although patients that achieved an objective tumor response exhibited Spn levels similar to nontumoral tissue, nonresponding patients showed a significant reduction in Spn mRNA levels.-
dc.description.abstract[Conclusions] Our data suggest that Spn downregulation contributes to a more aggressive biologic behavior, induces chemoresistance, and is associated with a poorer survival in patients with advanced stages of colorectal carcinoma. © 2013 American Association for Cancer Research.-
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministry of Science and Innovation (SAF2009-08605), Fondo de Investigacion Sanitaria (PI12/00137), Consejeria de Ciencia e Innovacion, and Consejeria de Salud of the Junta de Andalucia (CTS-6844 and PI-0142). A. Carnero's laboratory is also funded by a fellowship from Fundacion Oncologica FERO. P. Estevez-Garcia and I. Lopez-Calderero are supported by Rio Ortega Fellowships and S. Molina-Pinelo is supported by a Sara Borrell fellowship. R. Garcia-Carbonero is funded by the Instituto de Salud Carlos III, Ministerio de Sanidad, Spain (PI 10.02164).-
dc.publisherAmerican Association for Cancer Research-
dc.rightsclosedAccess-
dc.titleSpinophilin loss correlates with poor patient prognosis in advanced stages of colon carcinoma-
dc.typeartículo-
dc.identifier.doi10.1158/1078-0432.CCR-13-0057-
dc.relation.publisherversionhttp://doi.org/10.1158/1078-0432.CCR-13-0057-
dc.date.updated2017-01-30T11:01:10Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderJunta de Andalucía-
dc.contributor.funderFundación Fero-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004837es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100011011es_ES
item.fulltextNo Fulltext-
item.openairetypeartículo-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
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