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E-GEOD-42001 - Diverse phospho-signaling networks mediate RTK dependent growth and survival in childhood ALL [gene expression]

Status
Released on 3 November 2014, last updated on 8 November 2014
Organism
Homo sapiens
Samples (24)
Array (1)
Protocols (7)
Description
Deregulated RTK activity has been implicated as a causal leukemogenic factor in the context of molecular aberrations that perturb differentiation in the hematopoietic lineage such as in childhood ALL. A deeper understanding of RTK signaling processes on a system-wide scale will be key in defining critical components of signaling networks. To link RTK activity with in vivo output in primary ALL we took a functional approach, which combined SH2 domain binding, mass spectrometry, and transcriptome analyses. Structure and composition of evolving networks were highly diverse with few generic features determined by receptor and cell type. A combinatorial assembly of varying context-dependent and few generic signaling components at multiple levels likely generates output specificity. PAK2 was identified as a phosphoregulated FLT3 target, whose allosteric inhibition resulted in apoptosis of ALL cells. Our studies provide evidence that a functional approach to leukemia signaling may yield valuable information for a network-directed intervention. Three different primary ALL samples expressing FLT3 and/or PDGFRß were stimulated with the corresponding ligands FLT3L and PDGF-BB for five time points. Unstimulated samples served as control. ALL22089 coexpresses FLT3 and PDGFRß. ALL109 expresses PDGFRß. ALL114 expresses FLT3.
Experiment type
transcription profiling by array 
Contacts
Thomas Streichert <geo@ncbi.nlm.nih.gov>, Kevin Dierck, Martin Horstmann
MIAME
PlatformsProtocolsVariablesProcessedRaw
Files
Investigation descriptionE-GEOD-42001.idf.txt
Sample and data relationshipE-GEOD-42001.sdrf.txt
Raw data (1)E-GEOD-42001.raw.1.zip
Processed data (1)E-GEOD-42001.processed.1.zip
Array designA-AFFY-44.adf.txt
Links