Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/107377
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dc.contributor.authorAlves, Raquel-
dc.contributor.authorGonçalves, Ana Cristina-
dc.contributor.authorJorge, Joana-
dc.contributor.authorMarques, Gilberto João Padilha-
dc.contributor.authorLuís, Dino-
dc.contributor.authorRibeiro, André B.-
dc.contributor.authorTavares, Paulo-
dc.contributor.authorOliveiros, Bárbara-
dc.contributor.authorAlmeida, António M.-
dc.contributor.authorRibeiro, Ana Bela Sarmento-
dc.date.accessioned2023-07-06T11:07:14Z-
dc.date.available2023-07-06T11:07:14Z-
dc.date.issued2019-07-04-
dc.identifier.issn2045-2322pt
dc.identifier.urihttps://hdl.handle.net/10316/107377-
dc.description.abstractmicroRNAs (miRs) dysregulation have emerged as a crucial step in tumorigenesis, being related with cancer development, progression and response to treatment. In chronic myeloid leukaemia (CML), the resistance to tyrosine kinase inhibitors (TKI) is responsible for treatment failure and could be linked to changes in miRs expression. This work aimed to correlate the expression levels of 3 miRs, miR-21, miR-26b and miR-451, with response to TKI treatment in CML patients. miR-451 levels at diagnosis were significantly higher in patients with optimal response after 6 and 12 months of therapy. Conversely, patients without optimal response had highest levels of miR-21. miR-21 and miR-451 appear to be good biomarkers of response, able to predict optimal TKI responders (p < 0.05). Using the combined profile of both miRs, we create a predictive model of optimal response after one year of treatment. This study highlights the role of miR-21 and miR-451 expression levels at diagnosis in predicting which patients achieve the optimal response.pt
dc.language.isoengpt
dc.publisherSpringer Naturept
dc.relationSFRH/ BD/51994/2012pt
dc.relationCIMAGO (Project 10/14), by Faculty of Medicine of the University of Coimbra and Santander Totta Bank with the grant (FMUC-BST-2016-214)pt
dc.relationFCT/ MCTES/PIDDAC (CNC.IBILI. Centre Reference: UID/NEU/04539/2013)pt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subject.meshAdultpt
dc.subject.meshAgedpt
dc.subject.meshBiomarkers, Tumorpt
dc.subject.meshCell Transformation, Neoplasticpt
dc.subject.meshDisease Progressionpt
dc.subject.meshFemalept
dc.subject.meshFollow-Up Studiespt
dc.subject.meshGene Expression Regulation, Leukemicpt
dc.subject.meshHumanspt
dc.subject.meshImatinib Mesylatept
dc.subject.meshLeukemia, Myelogenous, Chronic, BCR-ABL Positivept
dc.subject.meshMalept
dc.subject.meshMicroRNAspt
dc.subject.meshMiddle Agedpt
dc.subject.meshPrognosispt
dc.subject.meshProtein Kinase Inhibitorspt
dc.subject.meshSurvival Ratept
dc.subject.meshTumor Cells, Culturedpt
dc.subject.meshDrug Resistance, Neoplasmpt
dc.titleMicroRNA signature refine response prediction in CMLpt
dc.typearticle-
degois.publication.firstPage9666pt
degois.publication.issue1pt
degois.publication.titleScientific Reportspt
dc.peerreviewedyespt
dc.identifier.doi10.1038/s41598-019-46132-9pt
degois.publication.volume9pt
dc.date.embargo2019-07-04*
uc.date.periodoEmbargo0pt
item.openairetypearticle-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.fulltextCom Texto completo-
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0003-2599-6433-
crisitem.author.orcid0000-0003-1470-4802-
crisitem.author.orcid0000-0001-7832-4134-
crisitem.author.orcid0000-0001-7836-8161-
crisitem.author.orcid0000-0002-4142-4841-
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
I&D ICBR - Artigos em Revistas Internacionais
FMUC Medicina - Artigos em Revistas Internacionais
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