Mechanisms of Glucocorticoid Response and Resistance in Lymphoid Malignancies

  • Lauren K. Meyer
  • Michelle L. HermistonEmail author
Part of the Resistance to Targeted Anti-Cancer Therapeutics book series (RTACT, volume 21)


Glucocorticoids (GC) are an integral component of multi-agent therapy regimens for a wide variety of lymphoid malignancies due to their potential effects to induce apoptosis in cells of the lymphoid lineage. Despite their clinical utility, de novo and acquired resistance to GC is a significant clinical problem that contributes to inferior outcomes for many of these diseases. This review summarizes what is currently known about mechanisms of GC resistance in lymphoid malignancies, with a particular focus on novel therapeutic strategies currently in preclinical or clinical development that are rationally-designed to overcome GC resistance and improve clinical outcomes.


Apoptosis Glucocorticoid Leukemia Lymphoma Metabolism MicroRNA Drug resistance Signal transduction 





3’ Untranslated Region


B-Cell Chronic Lymphocytic Leukemia




Cyclic Adenosine Monophosphate


Cyclin Dependent Kinase


Chromatin Immunoprecipitation with Sequencing


Cyclophosphamide, Adriamycin, Vincristine, and Prednisone


DNA Binding Domain




Diffuse Large B-Cell Lymphoma


Event-Free Survival




Glucocorticoid Receptor


Glucocorticoid Response Element


Glutathione S-Transferase


Histone Deacetylase


Hydroxysteroid Dehydrogenase


Ligand Binding Domain


Loss of Heterozygosity


Mitogen Activated Protein Kinase




Minimal Residual Disease


Nuclear Co-Receptor


Non-Hodgkin Lymphoma


N-Terminal Transactivation Domain




Patient-Derived Xenograft


Prednisone Good Responder


Protein Kinase A


Prednisone Poor Responder


Real-Time Polymerase Chain Reaction


T-Cell Acute Lymphoblastic Leukemia


T-Cell Receptor


White Blood Cell



L.K.M. is supported by the UCSF Medical Scientist Training Program Grant T32 GM007618 and by a Genentech Foundation Award. M.L.H is supported by the National Cancer Institute Grant R01 CA193776, The Campini Foundation, The Buster Posey Family Foundation, and The Pepp Family Foundation. The authors thank Kevin Shannon and Anica Wandler for their critical reading of the manuscript.

Disclosure of Conflict of Interest

No potential conflicts of interest were disclosed.


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© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of PediatricsUniversity of CaliforniaSan FranciscoUSA

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