Molecular mechanisms regulating glucocorticoid sensitivity and resistance

Katherine L. Gross, Nick Z. Lu, John A. Cidlowski*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

138 Scopus citations

Abstract

Glucocorticoid receptor agonists are mainstays in the treatment of various malignancies of hematological origin. Glucocorticoids are included in therapeutic regimens for their ability to stimulate intracellular signal transduction cascades that culminate in alterations in the rate of transcription of genes involved in cell cycle progression and programmed cell death. Unfortunately, subpopulations of patients undergoing systemic glucocorticoid therapy for these diseases are or become insensitive to glucocorticoid-induced cell death, a phenomenon recognized as glucocorticoid resistance. Multiple factors contributing to glucocorticoid resistance have been identified. Here we summarize several of these mechanisms and describe the processes involved in generating a host of glucocorticoid receptor isoforms from one gene. The potential role of glucocorticoid receptor isoforms in determining cellular responsiveness to glucocorticoids is emphasized.

Original languageEnglish (US)
Pages (from-to)7-16
Number of pages10
JournalMolecular and Cellular Endocrinology
Volume300
Issue number1-2
DOIs
StatePublished - Mar 5 2009

Keywords

  • Alternative initiation of translation
  • Glucocorticoid receptor
  • Glucocorticoid resistance
  • Hematological malignancy

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

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