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Resistance to tyrosine kinase inhibitors in chronic myeloid leukemia — from molecular mechanisms to clinical relevance

2021-10-01Journal article Open access
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dc.contributor.authorAlves, Raquel
dc.contributor.authorGonçalves, Ana Cristina
dc.contributor.authorRutella, Sergio
dc.contributor.authorAlmeida, António M.
dc.contributor.authorRivas, Javier De Las
dc.contributor.authorTrougakos, Ioannis P.
dc.contributor.authorRibeiro, Ana Bela Sarmento
dc.date.accessioned2021-10-04T15:20:46Z
dc.date.available2021-10-04T15:20:46Z
dc.date.issued2021-10-01
dc.description.abstractResistance to targeted therapies is a complex and multifactorial process that culminates in the selection of a cancer clone with the ability to evade treatment. Chronic myeloid leukemia (CML) was the first malignancy recognized to be associated with a genetic alteration, the t(9;22)(q34;q11). This translocation originates the BCR-ABL1 fusion gene, encoding the cytoplasmic chimeric BCR-ABL1 protein that displays an abnormally high tyrosine kinase activity. Although the vast majority of patients with CML respond to Imatinib, a tyrosine kinase inhibitor (TKI), resistance might occur either de novo or during treatment. In CML, the TKI resistance mechanisms are usually subdivided into BCR-ABL1-dependent and independent mechanisms. Furthermore, patients’ compliance/adherence to therapy is critical to CML management. Techniques with enhanced sensitivity like NGS and dPCR, the use of artificial intelligence (AI) techniques, and the development of mathematical modeling and computational prediction methods could reveal the underlying mechanisms of drug resistance and facilitate the design of more effective treatment strategies for improving drug efficacy in CML patients. Here we review the molecular mechanisms and other factors involved in resistance to TKIs in CML and the new methodologies to access these mechanisms, and the therapeutic approaches to circumvent TKI resistance.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.3390/cancers13194820pt_PT
dc.identifier.eid85115641235
dc.identifier.issn2072-6694
dc.identifier.pmcPMC8508378
dc.identifier.pmid34638304
dc.identifier.urihttp://hdl.handle.net/10400.14/35386
dc.identifier.wos000707334800001
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectBioinformatics and artificial intelligencept_PT
dc.subjectCMLpt_PT
dc.subjectEpigeneticspt_PT
dc.subjectImmune systempt_PT
dc.subjectNew targeted therapiespt_PT
dc.subjectPatient adherencept_PT
dc.subjectTKI resistancept_PT
dc.titleResistance to tyrosine kinase inhibitors in chronic myeloid leukemia — from molecular mechanisms to clinical relevancept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue19pt_PT
oaire.citation.titleCancerspt_PT
oaire.citation.volume13pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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