Unknown,Transcriptomics,Genomics,Proteomics

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Human T-ALL cell line response to inhibition of Notch signaling


ABSTRACT: Analysis of five Notch signaling-dependent human T-ALL cell lines (ALLSIL, DND41, HPBALL, KOPTK1, TALL-1) treated with gamma-secretase inhibitor (GSI) to block Notch signaling. Samples include parental cells, cells rescued by retroviral transduction with ICN (a GSI-independent form of activated Notch1), and cells retrovirally transduced with c-Myc (an important downstream target of Notch1). Results allow segregation of bona fide Notch targets from other genes affected by gamma-secretase inhibition as well as from targets downstream of c-Myc. Thirty samples were analyzed. Five human T-ALL cell lines (ALLSIL, DND41, HPBALL, KOPTK1, TALL-1) were treated with gamma-secretase inhibitor (1.0 micromolar compound E) vs. DMSO vehicle control for 12 hours. Each cell line was also retrovirally transduced with ICN or c-Myc, FACS sorted, and then treated with GSI vs. DMSO.

ORGANISM(S): Homo sapiens

SUBMITTER: Andrew Weng 

PROVIDER: E-GEOD-29959 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

High-level IGF1R expression is required for leukemia-initiating cell activity in T-ALL and is supported by Notch signaling.

Medyouf Hind H   Gusscott Samuel S   Wang Hongfang H   Tseng Jen-Chieh JC   Wai Carol C   Nemirovsky Oksana O   Trumpp Andreas A   Pflumio Francoise F   Carboni Joan J   Gottardis Marco M   Pollak Michael M   Kung Andrew L AL   Aster Jon C JC   Holzenberger Martin M   Weng Andrew P AP  

The Journal of experimental medicine 20110801 9


T cell acute lymphoblastic leukemia (T-ALL) is an aggressive cancer of immature T cells that often shows aberrant activation of Notch1 and PI3K-Akt pathways. Although mutations that activate PI3K-Akt signaling have previously been identified, the relative contribution of growth factor-dependent activation is unclear. We show here that pharmacologic inhibition or genetic deletion of insulin-like growth factor 1 receptor (IGF1R) blocks the growth and viability of T-ALL cells, whereas moderate dimi  ...[more]

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