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Genetic biomarkers in chronic myeloid leukemia

2021-11-19Recensão Acesso aberto
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dc.contributor.authorAbdulmawjood, Bilal
dc.contributor.authorCosta, Beatriz
dc.contributor.authorRoma-Rodrigues, Catarina
dc.contributor.authorBaptista, Pedro V.
dc.contributor.authorFernandes, Alexandra R.
dc.contributor.institutionDCV - Departamento de Ciências da Vida
dc.contributor.institutionUCIBIO - Applied Molecular Biosciences Unit
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2022-03-21T23:26:28Z
dc.date.available2022-03-21T23:26:28Z
dc.date.issued2021-11-19
dc.descriptionUIDP/04378/2020 UIDB/04378/2020 LA/P/0140/2020
dc.description.abstractChronic Myeloid Leukemia (CML) is a rare malignant proliferative disease of the hematopoietic system, whose molecular hallmark is the Philadelphia chromosome (Ph). The Ph chromosome originates an aberrant fusion gene with abnormal kinase activity, leading to the buildup of reactive oxygen species and genetic instability of relevance in disease progression. Several genetic abnormalities have been correlated with CML in the blast phase, including chromosomal aberrations and common altered genes. Some of these genes are involved in the regulation of cell apoptosis and proliferation, such as the epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), or Schmidt-Ruppin A-2 proto-oncogene (SRC); cell adhesion, e.g., catenin beta 1(CTNNB1); or genes associated to TGF-β, such as SKI like proto-oncogene (SKIL), transforming growth factor beta 1 (TGFB1) or transforming growth factor beta 2 (TGFB2); and TNF-α pathways, such as Tumor necrosis factor (TNFA) or Nuclear factor kappa B subunit 1 (NFKB1). The involvement of miRNAs in CML is also gaining momentum, where dysregulation of some critical miRNAs, such as miRNA-451 and miRNA-21, which have been associated to the molecular modulation of pathogenesis, progression of disease states, and response to therapeutics. In this review, the most relevant genomic alterations found in CML will be addressed.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent23
dc.format.extent1640171
dc.identifier.doi10.3390/ijms222212516
dc.identifier.issn1661-6596
dc.identifier.otherPURE: 42510136
dc.identifier.otherPURE UUID: 0edd584b-f65d-4bda-8c19-1d5dc1d2c8f9
dc.identifier.otherScopus: 85119247211
dc.identifier.otherPubMed: 34830398
dc.identifier.otherPubMedCentral: PMC8626020
dc.identifier.otherWOS: 000725165300001
dc.identifier.urihttp://hdl.handle.net/10362/134978
dc.identifier.urlhttps://www.scopus.com/pages/publications/85119247211
dc.language.isoeng
dc.peerreviewedyes
dc.subjectChronic myeloid leukemia
dc.subjectGenetic biomarkers
dc.subjectGenomic instability
dc.subjectMiRNAs
dc.subjectPhiladelphia chromosome
dc.subjectCatalysis
dc.subjectMolecular Biology
dc.subjectSpectroscopy
dc.subjectComputer Science Applications
dc.subjectPhysical and Theoretical Chemistry
dc.subjectOrganic Chemistry
dc.subjectInorganic Chemistry
dc.subjectSDG 3 - Good Health and Well-being
dc.titleGenetic biomarkers in chronic myeloid leukemiaen
dc.title.subtitleWhat have we learned so far?en
dc.typereview
degois.publication.issue22
degois.publication.titleInternational Journal of Molecular Sciences
degois.publication.volume22
dspace.entity.typePublication
rcaap.rightsopenAccess

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