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dc.contributor.authorMariscal, Javier
dc.contributor.authorAlonso Nocelo, Marta
dc.contributor.authorMuinelo Romay, Laura
dc.contributor.authorBarbazán García, Jorge
dc.contributor.authorVieito, María
dc.contributor.authorAbalo, Alicia
dc.contributor.authorGómez Tato, Antonio
dc.contributor.authorCasares de Cal, María Ángeles
dc.contributor.authorGarcía-Caballero Parada, Tomás
dc.contributor.authorRodríguez, Carmela
dc.contributor.authorBrozos, Elena
dc.contributor.authorBaron, Francisco
dc.contributor.authorLópez López, Rafael
dc.contributor.authorAbal Posada, Miguel
dc.date.accessioned2020-06-09T10:52:07Z
dc.date.available2020-06-09T10:52:07Z
dc.date.issued2016
dc.identifier.citationMariscal, J., Alonso-Nocelo, M., Muinelo-Romay, L. et al. Molecular Profiling of Circulating Tumour Cells Identifies Notch1 as a Principal Regulator in Advanced Non-Small Cell Lung Cancer. Sci Rep 6, 37820 (2016). https://doi.org/10.1038/srep37820
dc.identifier.urihttp://hdl.handle.net/10347/22923
dc.description.abstractKnowledge on the molecular mechanisms underlying metastasis colonization in Non-Small Cell Lung Cancer (NSCLC) remains incomplete. A complete overview integrating driver mutations, primary tumour heterogeneity and overt metastasis lacks the dynamic contribution of disseminating metastatic cells due to the inaccessibility to the molecular profiling of Circulating Tumour Cells (CTCs). By combining immunoisolation and whole genome amplification, we performed a global gene expression analysis of EpCAM positive CTCs from advanced NSCLC patients. We identified an EpCAM+ CTC-specific expression profile in NSCLC patients mostly associated with cellular movement, cell adhesion and cell-to-cell signalling mediated by PI3K/AKT, ERK1/2 and NF-kB pathways. NOTCH1 emerged as a driver connecting active signalling pathways, with a reduced number of related candidate genes (NOTCH1, PTP4A3, LGALS3 and ITGB3) being further validated by RT-qPCR on an independent cohort of NSCLC patients. In addition, these markers demonstrated high prognostic value for Progression-Free Survival (PFS). In conclusion, molecular characterization of EpCAM+ CTCs from advanced NSCLC patients provided with highly specific biomarkers with potential applicability as a “liquid biopsy” for monitoring of NSCLC patients and confirmed NOTCH1 as a potential therapeutic target to block lung cancer dissemination.
dc.description.sponsorshipThis work was funded by InveNNta (Innovation in Nanomedicine); Operational Programme for Cross-border Cooperation: Spain-Portugal (POCTEP) and European Regional Development Fund (ERDF). Javier Mariscal is recipient of a fellowship from Escola de Doutoramento Internacional Campus Vida of the University of Santiago de Compostela. Laura Muinelo-Romay is supported by ISCIII as Responsible of the Liquid Biopsy Analysis Unit
dc.language.isoeng
dc.publisherNature Publishing Group
dc.rights© The Author(s) 2016. Open Access. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectLung Cancer
dc.subjectMetastasis
dc.subjectCirculating Tumour Cells (CTCs)
dc.subjectLiquid biopsy
dc.subjectBiomarkers
dc.titleMolecular Profiling of Circulating Tumour Cells Identifies Notch1 as a Principal Regulator in Advanced Non-Small Cell Lung Cancer
dc.typejournal article
dc.identifier.doi10.1038/srep37820
dc.relation.publisherversionhttps://doi.org/10.1038/srep37820
dc.type.hasVersionVoR
dc.identifier.essn2045-2322
dc.rights.accessRightsopen access
dc.contributor.affiliationUniversidade de Santiago de Compostela. Departamento de Ciencias Morfolóxicas
dc.description.peerreviewedSI


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© The Author(s) 2016. Open Access. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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 © The Author(s) 2016. Open Access. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/





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