Decreased Expression of microRNA-451 is Associated with Imatinib Mesylate Resistance in Chronic Myeloid Leukemia Patients

Khalifa, Khaled A; Abbas, Omaima M; AbdlFattah, Raafat M.; Alhassanin, Suzan; Shehata, A.; Esawy, Sally

doi:10.1016/j.clml.2019.07.240

Cited by 1 publication

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“…This regulatory loop might be the basis of the up-regulation of miRNA-451 in CP CML patients who achieved MMR after IM treatment, compared to recently diagnosed CML-CP patients [161]. Moreover, miRNA-451 expression levels were also correlated with IM response, as its levels were downregulated in IM-resistant patients compared to IM-responsive or healthy controls [161]. Nevertheless, no significant variations were observed between IM-responsive and healthy control groups [161].…”

Section: Mirnas That Target Bcr-abl1mentioning

confidence: 96%

“…Moreover, miRNA-451 expression levels were also correlated with IM response, as its levels were downregulated in IM-resistant patients compared to IM-responsive or healthy controls [161]. Nevertheless, no significant variations were observed between IM-responsive and healthy control groups [161].…”

Section: Mirnas That Target Bcr-abl1mentioning

confidence: 99%

“…As its potential target is BCR-ABL1, the authors proposed the existence of a reciprocal regulatory loop between them, and that BCR-ABL1 inhibits miRNA-451, its negative regulator, to increase its expression and allow CML progression [168]. This regulatory loop might be the basis of the up-regulation of miRNA-451 in CP CML patients who achieved MMR after IM treatment, compared to recently diagnosed CML-CP patients [161]. Moreover, miRNA-451 expression levels were also correlated with IM response, as its levels were downregulated in IM-resistant patients compared to IM-responsive or healthy controls [161].…”

Section: Mirnas That Target Bcr-abl1mentioning

confidence: 99%

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

Abdulmawjood

Costa

Roma‐Rodrigues

et al. 2021

IJMS

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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 (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.

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Section: Mirnas That Target Bcr-abl1mentioning

confidence: 96%

Section: Mirnas That Target Bcr-abl1mentioning

confidence: 99%