ArticleGenomics2003
Gene expression profile of human lymphoid CEM cells sensitive and resistant to glucocorticoid-evoked apoptosis.
Article in Genomics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed.
- A Coumarin-Imidazothiadiazole Derivative, SP11 Abrogates Tumor Growth by Targeting HSP90 and Its Client Proteins.Molecules (Basel, Switzerland) · 2023Article
- Dexamethasone-Induced Fatty Acid Oxidation and Autophagy/Mitophagy Are Essential for T-ALL Glucocorticoid Resistance.Cancers · 2023Article
- Dexamethasone enhances glucose uptake by SGLT1 and GLUT1 and boosts ATP generation through the PPP-TCA cycle in bovine neutrophils.Journal of veterinary science · 2022Article
- Gasdermin E-mediated programmed cell death: An unpaved path to tumor suppression.Journal of Cancer · 2021Review
- Reversal of glucocorticoid resistance in paediatric acute lymphoblastic leukaemia is dependent on restoring BIM expression.British journal of cancer · 2020Article
- Influence of BCL2L11 polymorphism on osteonecrosis during treatment of childhood acute lymphoblastic leukemia.The pharmacogenomics journal · 2019Article
- Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells:interactions of MAPK, MYC and glucocorticoid pathways.Molecular and cellular endocrinology · 2018Review
- Effect of combining glucocorticoids with Compound A on glucocorticoid receptor responsiveness in lymphoid malignancies.PloS one · 2018Article
- Article
- Shift in energy metabolism caused by glucocorticoids enhances the effect of cytotoxic anti-cancer drugs against acute lymphoblastic leukemia cells.Oncotarget · 2017Article
- Article
- Restored mutant receptor:Corticoid binding in chaperone complexes by trimethylamine N-oxide.PloS one · 2017Article
- Glucocorticoid-mediated co-regulation of RCAN1-1, E4BP4 and BIM in human leukemia cells susceptible to apoptosis.Biochemical and biophysical research communications · 2015Article
- Correlation of glucocorticoid-mediated E4BP4 upregulation with altered expression of pro- and anti-apoptotic genes in CEM human lymphoblastic leukemia cells.Biochemical and biophysical research communications · 2014Article
- REDD1/DDIT4-independent mTORC1 inhibition and apoptosis by glucocorticoids in thymocytes.Molecular cancer research : MCR · 2014Article
- Epigenetic alteration by DNA-demethylating treatment restores apoptotic response to glucocorticoids in dexamethasone-resistant human malignant lymphoid cells.Cancer cell international · 2014Article
- Article
- MicroRNAs and Glucocorticoid-Induced Apoptosis in Lymphoid Malignancies.ISRN hematology · 2013Article
- Elucidating the identity of resistance mechanisms to prednisolone exposure in acute lymphoblastic leukemia cells through transcriptomic analysis: A computational approach.Journal of clinical bioinformatics · 2011Article
- Evaluation of the NOD/SCID xenograft model for glucocorticoid-regulated gene expression in childhood B-cell precursor acute lymphoblastic leukemia.BMC genomics · 2011Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Three closely related clones of leukemic lymphoid CEM cells were compared for their gene expression responses to the glucocorticoid dexamethasone (Dex). All three contained receptors for Dex, but only two responded by undergoing apoptosis. After a time of exposure to Dex that ended late in the interval preceding onset of apoptosis, gene microarray analyses were carried out. The results indicate that the expression of a limited, distinctive set of genes was altered in the two apoptosis-prone clones, not in the resistant clone. That clone showed altered expression of different sets of genes, suggesting that a molecular switch converted patterns of gene expression between the two phenotypes: apoptosis-prone and apoptosis-resistant. The results are consistent with the hypothesis that altered expression of a distinctive network of genes after glucocorticoid administration ultimately triggers apoptosis of leukemic lymphoid cells. The altered genes identified provide new foci for study of their role in cell death.
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Registered trials
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