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


Journal

Current drug research reviews
ISSN: 2589-9783
Titre abrégé: Curr Drug Res Rev
Pays: United Arab Emirates
ID NLM: 101735701

Informations de publication

Date de publication:
2020
Historique:
received: 02 10 2019
revised: 29 12 2019
accepted: 23 01 2020
pubmed: 23 2 2020
medline: 15 10 2021
entrez: 21 2 2020
Statut: ppublish

Résumé

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. 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. 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. 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. 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.

Sections du résumé

BACKGROUND 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 OBJECTIVE
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 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 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 CONCLUSIONS
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.

Identifiants

pubmed: 32077838
pii: CDRR-EPUB-104688
doi: 10.2174/2589977512666200220122650
doi:

Substances chimiques

Antineoplastic Agents 0
Glucocorticoids 0
Prednisolone 9PHQ9Y1OLM

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

131-149

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

George I Lambrou (GI)

First Department of Pediatrics, National and Kapodistrian University of Athens, Choremeio Research Laboratory, Athens, Greece.

Maria Adamaki (M)

First Department of Pediatrics, National and Kapodistrian University of Athens, Choremeio Research Laboratory, Athens, Greece.

Kyriaki Hatziagapiou (K)

First Department of Pediatrics, National and Kapodistrian University of Athens, Choremeio Research Laboratory, Athens, Greece.

Spiros Vlahopoulos (S)

First Department of Pediatrics, National and Kapodistrian University of Athens, Choremeio Research Laboratory, Athens, Greece.

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Classifications MeSH