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2010;182 1-30.

Glucocorticoid-induced apoptosis of healthy and malignant lymphocytes.

Lindsay K Smith, John A Cidlowski
Author Information
  1. Lindsay K Smith: Molecular Endocrinology Group, Laboratory of Signal Transduction, NIEHS, NIH, DHHS, Research Triangle Park, NC, USA.
PMID: 20541659 DOI: 10.1016/S0079-6123(10)82001-1

Abstract

Glucocorticoids exert a wide range of physiological effects, including the induction of apoptosis in lymphocytes. The progression of glucocorticoid-induced apoptosis is a multi-component process requiring contributions from both genomic and cytoplasmic signaling events. There is significant evidence indicating that the transactivation activity of the glucocorticoid receptor is required for the initiation of glucocorticoid-induced apoptosis. However, the rapid cytoplasmic effects of glucocorticoids may also contribute to the glucocorticoid-induced apoptosis-signaling pathway. Endogenous glucocorticoids shape the T-cell repertoire through both the induction of apoptosis by neglect during thymocyte maturation and the antagonism of T-cell receptor (TCR)-induced apoptosis during positive selection. Owing to their ability to induce apoptosis in lymphocytes, synthetic glucocorticoids are widely used in the treatment of haematological malignancies. Glucocorticoid chemotherapy is limited, however, by the emergence of glucocorticoid resistance. The development of novel therapies designed to overcome glucocorticoid resistance will dramatically improve the efficacy of glucocorticoid therapy in the treatment of haematological malignancies.

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Grants

  1. Z01 ES090079-12/Intramural NIH HHS

MeSH Term

Apoptosis
Gene Expression Regulation
Glucocorticoids
Hematologic Neoplasms
Humans
Lymphocytes
Lymphoma, Non-Hodgkin
Male
Models, Biological
Multiple Myeloma
Mutation
Receptors, Glucocorticoid
Signal Transduction

Chemicals

Glucocorticoids
Receptors, Glucocorticoid
Journal Article

Word Cloud

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