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<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="ownerprofile_id">arrayexpress_sid</item><item key="id">3681</item><item key="factors"><item><item key="GSM550942"><item key="Cell Line">C7H2-R10E7</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550943"><item key="Cell Line">C7H2-R19E5</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550944"><item key="Cell Line">C7H2-R9C10</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550945"><item key="Cell Line">C7H2-R3B5</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550946"><item key="Cell Line">C7H2-R19F2</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550947"><item key="Cell Line">C7H2-R19E7</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550948"><item key="Cell Line">C7H2-S11</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550949"><item key="Cell Line">C7H2-S12</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550950"><item key="Cell Line">C7H2-S27(ZR)</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM55095"><item key="Cell Line">C7H2-S10</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550952"><item key="Cell Line">C7H2-S2</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550953"><item key="Cell Line">C7H2-S15</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">vehicle</item></item></item><item><item key="GSM550954"><item key="Cell Line">C7H2-R10E7</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550955"><item key="Cell Line">C7H2-R19E5</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550956"><item key="Cell Line">C7H2-R9C10</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550957"><item key="Cell Line">C7H2-R3B5</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550958"><item key="Cell Line">C7H2-R19F2</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550959"><item key="Cell Line">C7H2-R19E7</item><item key="Phenotype">glucocorticoid resistant</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550960"><item key="Cell Line">C7H2-S11</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM55096"><item key="Cell Line">C7H2-S12</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550962"><item key="Cell Line">C7H2-S27</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550963"><item key="Cell Line">C7H2-S10</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550964"><item key="Cell Line">C7H2-S2</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">dexamethasone</item></item></item><item><item key="GSM550965"><item key="Cell Line">C7H2-S15</item><item key="Phenotype">glucocorticoid sensitive</item><item key="Treatment">dexamethasone</item></item></item></item><item key="pop_total">0</item><item key="platform">4</item><item key="summary_wrapped">Gene expression data of glucocorticoid resistant and sensitive acute lymphoblastic leukemia cell lines for the article: Expression,...</item><item key="pubmed_id">21092265</item><item key="geo_gse_id">E-GEOD-22152</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">3</item><item key="sample_count">24</item><item key="tags"><item>acute lymphoblastic leukemia</item><item>cell</item><item>central</item><item>glucose</item><item>leukemia</item><item>line</item><item>lymphoblastic leukemia</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_id_plat">E-GEOD-22152_A-AFFY-44</item><item key="slug">transcription-profiling-of-glucocorticoid-resistan</item><item key="geo_gds_id"/><item key="name">Transcription profiling of glucocorticoid resistant and sensitive acute lymphoblastic leukemia cell lines</item><item key="created">Sep.15, 2014</item><item key="summary">Gene expression data of glucocorticoid resistant and sensitive acute lymphoblastic leukemia cell lines for the article: Expression, regulation and function of phosphofructo-kinase/fructose-biphosphatases  (PFKFBs) in glucocorticoid-induced apoptosis of acute lymphoblastic leukemia cells  Glucocorticoids (GCs) cause apoptosis and cell cycle arrest in lymphoid cells and constitute a central component in the therapy of lymphoid malignancies, most notably childhood acute lymphoblastic leukemia (ALL). PFKFB2 (6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-2), a kinase controlling glucose metabolism, was identified by us previously as GC response gene in expression profiling analyses performed in children with ALL during initial systemic GC mono-therapy. Since deregulation of glucose metabolism has been implicated in apoptosis induction, this gene and its relatives PFKFB1, 3, and 4 were further analyzed. Expression analyses in additional ALL children, non-leukemic individuals and leukemic cell lines confirmed frequent PFKFB2 induction by GC in most systems sensitive to GC-induced apoptosis, particularly in T-ALL cells. The 3 other family members, in contrast, were not or weakly expressed (PFKFB1 and 4) or not induced by GC (PFKFB3). Conditional PFKFB2 over-expression in the CCRF-CEM T-ALL in vitro model revealed that its 2 splice variants (15A and 15B) did not have any detectable effect on survival or cell cycle progression. Moreover, neither PFKFB2 splice variant significantly affected sensitivity to, or kinetics of, GC-induced apoptosis. Our data suggest that, at least in the model system investigated, PFKFB2 is not an essential upstream regulator of the anti-leukemic effects of GC. Generation of the GC sensitive and resistant clones is described in Parson et al. FASEB J 2005 (Pubmed id 15637111). In brief GC sensitive clones were generated by limiting dilution subcloning from the GC sensitive T-ALL cell line CCRF-CEM-C7H2. To generate GC resistant clones the CCRF-CEM-C7H2 cell line was clutured in the presence of 10E-7 M dexametasone. Gene expression profiles of glucocorticoid (GC) resistant and sensitive T-ALL cells during GC treatment and corresponding control samples (cells treated with carrier control). GC induced regulation of PFKFB2 was determined in the various cell lines based on the expression intensities of the corresponding probe sets in GC treated and control samples.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22152</item><item key="species">human</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22152/samples/</item></data></biogps>
