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Current Drug Research Reviews


ISSN (Print): 2589-9775
ISSN (Online): 2589-9783

Review Article

Gene Expression and Resistance to Glucocorticoid-Induced Apoptosis in Acute Lymphoblastic Leukemia: A Brief Review and Update

Author(s): George I. Lambrou*, Maria Adamaki , Kyriaki Hatziagapiou and Spiros Vlahopoulos*

Volume 12, Issue 2, 2020

Page: [131 - 149] Pages: 19

DOI: 10.2174/2589977512666200220122650

Price: $65


Background: Resistance to glucocorticoid (GC)-induced apoptosis in Acute Lymphoblastic Leukemia (ALL), is considered one of the major prognostic factors for the disease. Prednisolone 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 focuses on this topic.

Aim: The aim of the present study is to review some aspects of GC resistance in ALL, and in particular 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 retrieved.

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.

Keywords: Glucocorticoids, prednisolone, acute lymphoblastic leukemia, glucocorticoid-induced apoptosis resistance, apoptosis, gene expression, RelA.

Graphical Abstract
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