Τίτλος:
Gene expression and resistance to glucocorticoid-induced apoptosis in acute lymphoblastic leukemia: A brief review and update
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Background: Resistance to glucocorticoid (GC)-induced apoptosis in Acute Lympho-blastic Leukemia (ALL), is considered one of the major prognostic factors for the disease. Predniso-lone is a corticosteroid and one of the most important agents in the treatment of acute lymphoblastic leukemia. The mechanics of GC resistance are largely unknown and intense ongoing research focus-es on this topic. Aim: The aim of the present study is to review some aspects of GC resistance in ALL, and in partic-ular of Prednisolone, with emphasis on previous and present knowledge on gene expression and signaling pathways playing a role in the phenomenon. Methods: An electronic literature search was conducted by the authors from 1994 to June 2019. Original articles and systematic reviews selected, and the titles and abstracts of papers screened to determine whether they met the eligibility criteria, and full texts of the selected articles were re-trieved. Results: Identification of gene targets responsible for glucocorticoid resistance may allow discovery of drugs, which in combination with glucocorticoids may increase the effectiveness of anti-leukemia therapies. The inherent plasticity of clinically evolving cancer justifies approaches to characterize and prevent undesirable activation of early oncogenic pathways. Conclusion: Study of the pattern of intracellular signal pathway activation by anticancer drugs can lead to development of efficient treatment strategies by reducing detrimental secondary effects. © 2020 Bentham Science Publishers.
Συγγραφείς:
Lambrou, G.I.
Adamaki, M.
Hatziagapiou, K.
Vlahopoulos, S.
Περιοδικό:
Current Drug Research Reviews
Εκδότης:
Bentham Science Publishers
Λέξεις-κλειδιά:
cytidine deaminase; deoxycytidine kinase; dihydrofolate reductase inhibitor; eleven nineteen leukemia protein; epidermal growth factor; gammaglutamyl hydrolase; glucocorticoid; glucocorticoid receptor; immunoglobulin enhancer binding protein; methotrexate; multidrug resistance protein 1; myoglobin; nilotinib; phosphatidylinositol 3 kinase; prednisolone; reactive oxygen metabolite; small interfering RNA; transcription factor; transcription factor CP2; transcription factor RelA; unclassified drug; zinc finger with interaction domain; antineoplastic agent; glucocorticoid; prednisolone, acute lymphoblastic leukemia; apoptosis; cancer resistance; drug efficacy; gene expression; genetic polymorphism; human; mitochondrial membrane potential; myofibroblast; nervous system development; nonhuman; osteoclastogenesis; oxidative phosphorylation; oxidative stress; regulatory T lymphocyte; Review; signal transduction; single nucleotide polymorphism; acute lymphoblastic leukemia; animal; apoptosis; drug effect; drug resistance; gene expression regulation; genetics; pathology, Animals; Antineoplastic Agents; Apoptosis; Drug Resistance, Neoplasm; Gene Expression Regulation, Neoplastic; Glucocorticoids; Humans; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Prednisolone; Signal Transduction
DOI:
10.2174/2589977512666200220122650
