Authors: Shlomit KfirErenfeld Eitan Yefenof
Publish Date: 2013/09/26
Volume: 63, Issue: 1, Pages: 37-43
Abstract
Glucocorticoid GC hormones have been introduced as therapeutic agents in blood cancers six decades ago The effectiveness of GC treatment stems from its ability to induce apoptotic death of hemopoietic cells A major impediment in GC therapy is the acquisition of resistance to the drug upon repeated treatment In addition some blood cancers are a priori resistant to GC therapy Usually resistance to GC correlates with poor prognosis Albeit the wide use of GC in clinical practice their mode of action is not fully understood The cellular response to GC is initiated by its binding to the cytosolic GC receptor GR that translocates to the nucleus and modulates gene expression However nuclear activities of GR occur in both apoptosissensitive and apoptosisresistant cells These apparent controversies can be resolved by deciphering nongenomic effects of GCs and the mode by which they modulate the apoptotic response We suggest that nongenomic consequences of GC stimulation determine the cell fate toward survival or death Understanding the cellular mechanisms of GC apoptotic sensitivity contributes to the development of new modalities for overcoming GC resistanceThis paper is a Focussed Research Review based on a presentation given at the Third International Conference on Cancer Immunotherapy and Immunomonitoring CITIM 2013 held in Krakow Poland 22nd–25th April 2013 It is part of a CII series of Focussed Research Reviews and meeting report
Keywords: