Gene expression profiles of proliferating vs. G1/G0 arrested human leukemia cells suggest a mechanism for glucocorticoid‐induced apoptosis

@article{Tonko2001GeneEP,
  title={Gene expression profiles of proliferating vs. G1/G0 arrested human leukemia cells suggest a mechanism for glucocorticoid‐induced apoptosis},
  author={M. Tonko and Michael J. Ausserlechner and David Bernhard and Arno Helmberg and Reinhard Kofler},
  journal={The FASEB Journal},
  year={2001},
  volume={15},
  pages={693 - 699}
}
Glucocorticoids (GC) have pronounced effects on metabolism, differentiation, proliferation, and cell survival (1). In certain lymphocytes and lymphocyte‐related malignancies, GC inhibit proliferation and induce apoptotic cell death, which has led to their extensive use in the therapy of malignant lymphoproliferative disorders (2). Most of these effects result from regulation of gene expression via the GC receptor (GR), a ligand‐activated transcription factor (3). Although hundreds of genes are… 
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Analysis of gene expression patterns during glucocorticoid-induced apoptosis using oligonucleotide arrays.
Glucocorticoid-induced apoptosis and glucocorticoid resistance in acute lymphoblastic leukemia
Identification of genes leading to glucocorticoid-induced leukemic cell death
TLDR
Gene microarray analysis found the network of genes involved in GC-evoked cell death, using three clones derived from the CEM lymphoid leukemia cell line, and suggested that primary gene targets for GC often lack a classic GC response element.
Granzyme A mediates glucocorticoid‐induced apoptosis in leukemia cells
TLDR
Results showed that granzyme A is critically involved in mediating the apoptotic effect of glucocorticoid on leukemia cells, and the granzyme inhibitor 3,4‐dichloroisocoumarin inhibited the dexamethasone‐induced apoptosis of 697 cells in a concentration‐dependent manner.
Cyclin D3 and c-MYC control glucocorticoid-induced cell cycle arrest but not apoptosis in lymphoblastic leukemia cells
TLDR
It is suggested that repression of both, c-myc and cyclin D3, is necessary to arrest human leukemia cells in the G1 phase of the cell division cycle, but that neither one is required for GC-induced apoptosis.
Expression profiling of glucocorticoid-treated T-ALL cell lines: rapid repression of multiple genes involved in RNA-, protein- and nucleotide synthesis
TLDR
Several genes were found to be regulated that may contribute to synergistic action of glucocorticoid component of chemotherap#y protocols with other components of frequently used chemotherapy protocols such as antimetabolites, methotrexate and alkylating agents.
Mechanisms regulating the susceptibility of hematopoietic malignancies to glucocorticoid-induced apoptosis.
Gene expression profile of human lymphoid CEM cells sensitive and resistant to glucocorticoid-evoked apoptosis.
Cell-specific regulation of apoptosis by glucocorticoids: implication to their anti-inflammatory action.
Gene networks in glucocorticoid-evoked apoptosis of leukemic cells
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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