Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?

Chronic 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 an...

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Autores principales:	Bilal Abdulmawjood, Beatriz Costa, Catarina Roma-Rodrigues, Pedro V. Baptista, Alexandra R. Fernandes
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	chronic myeloid leukemia Philadelphia chromosome genetic biomarkers miRNAs genomic instability Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/6aeb2d806be14f6892b1b842b6752cf0
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spelling	oai:doaj.org-article:6aeb2d806be14f6892b1b842b6752cf02021-11-25T17:57:25ZGenetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?10.3390/ijms2222125161422-00671661-6596https://doaj.org/article/6aeb2d806be14f6892b1b842b6752cf02021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12516https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Chronic 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 (<i>EGFR</i>)<i>,</i> tumor protein p53 (<i>TP53</i>), or Schmidt-Ruppin A-2 proto-oncogene (<i>SRC</i>); cell adhesion, e.g., catenin beta 1 (<i>CTNNB1</i>); or genes associated to TGF-β, such as SKI like proto-oncogene (<i>SKIL</i>), transforming growth factor beta 1 (<i>TGFB1</i>) or transforming growth factor beta 2 (<i>TGFB2</i>); and TNF-α pathways, such as Tumor necrosis factor (<i>TNFA</i>) or Nuclear factor kappa B subunit 1 (<i>NFKB1</i>). 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.Bilal AbdulmawjoodBeatriz CostaCatarina Roma-RodriguesPedro V. BaptistaAlexandra R. FernandesMDPI AGarticlechronic myeloid leukemiaPhiladelphia chromosomegenetic biomarkersmiRNAsgenomic instabilityBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12516, p 12516 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	chronic myeloid leukemia Philadelphia chromosome genetic biomarkers miRNAs genomic instability Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	chronic myeloid leukemia Philadelphia chromosome genetic biomarkers miRNAs genomic instability Biology (General) QH301-705.5 Chemistry QD1-999 Bilal Abdulmawjood Beatriz Costa Catarina Roma-Rodrigues Pedro V. Baptista Alexandra R. Fernandes Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
description	Chronic 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 (<i>EGFR</i>)<i>,</i> tumor protein p53 (<i>TP53</i>), or Schmidt-Ruppin A-2 proto-oncogene (<i>SRC</i>); cell adhesion, e.g., catenin beta 1 (<i>CTNNB1</i>); or genes associated to TGF-β, such as SKI like proto-oncogene (<i>SKIL</i>), transforming growth factor beta 1 (<i>TGFB1</i>) or transforming growth factor beta 2 (<i>TGFB2</i>); and TNF-α pathways, such as Tumor necrosis factor (<i>TNFA</i>) or Nuclear factor kappa B subunit 1 (<i>NFKB1</i>). 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.
format	article
author	Bilal Abdulmawjood Beatriz Costa Catarina Roma-Rodrigues Pedro V. Baptista Alexandra R. Fernandes
author_facet	Bilal Abdulmawjood Beatriz Costa Catarina Roma-Rodrigues Pedro V. Baptista Alexandra R. Fernandes
author_sort	Bilal Abdulmawjood
title	Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
title_short	Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
title_full	Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
title_fullStr	Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
title_full_unstemmed	Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
title_sort	genetic biomarkers in chronic myeloid leukemia: what have we learned so far?
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/6aeb2d806be14f6892b1b842b6752cf0
work_keys_str_mv	AT bilalabdulmawjood geneticbiomarkersinchronicmyeloidleukemiawhathavewelearnedsofar AT beatrizcosta geneticbiomarkersinchronicmyeloidleukemiawhathavewelearnedsofar AT catarinaromarodrigues geneticbiomarkersinchronicmyeloidleukemiawhathavewelearnedsofar AT pedrovbaptista geneticbiomarkersinchronicmyeloidleukemiawhathavewelearnedsofar AT alexandrarfernandes geneticbiomarkersinchronicmyeloidleukemiawhathavewelearnedsofar
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Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?

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