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.