Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?
| العنوان: | Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far? |
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| المؤلفون: | Bilal R. Abdulmawjood, Catarina Roma-Rodrigues, Beatriz Costa, Pedro V. Baptista, Alexandra R. Fernandes |
| المصدر: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 22, Iss 12516, p 12516 (2021) |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | QH301-705.5, Proto-Oncogene Proteins pp60(c-src), Review, Biology, Philadelphia chromosome, Catalysis, Inorganic Chemistry, Fusion gene, Transforming Growth Factor beta1, chronic myeloid leukemia, hemic and lymphatic diseases, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, medicine, Biomarkers, Tumor, Humans, Epidermal growth factor receptor, Biology (General), Physical and Theoretical Chemistry, Kinase activity, QD1-999, Molecular Biology, Spectroscopy, beta Catenin, Organic Chemistry, Myeloid leukemia, General Medicine, Transforming growth factor beta, medicine.disease, genetic biomarkers, genomic instability, Computer Science Applications, ErbB Receptors, Chemistry, miRNAs, Cancer research, biology.protein, Catenin Beta-1, Tumor Suppressor Protein p53, Blast Crisis, Reactive Oxygen Species, Proto-oncogene tyrosine-protein kinase Src |
| الوصف: | 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. |
| تدمد: | 1422-0067 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a83c90db4163d95acee87418a0272e94 https://pubmed.ncbi.nlm.nih.gov/34830398 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....a83c90db4163d95acee87418a0272e94 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14220067 |
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