Dataset Information


Imatinib Treatment of GIST882

ABSTRACT: Gastrointestinal Stromal Tumor frequently harbor mutations in the KIT receptor tyrosine kinase and depend on its activity for growth. This underlies the efficacy of imatinib, a inhibitor of KIT activity, in GIST management. GIST882 is a patient derived GIST cell line that harbor a K640E exon 13 KIT mutation and is sensitive to imatinib treatment. To analyze the downstream effect of KIT inhibition, GIST882 cells were treated for 8 hours with 1μM Imatinib. GIST882 cells were treated in triplicate with 0.1% DMSO or 1μM Imatinib for 8 hours. RNA was isolated and analyzed by Illumina Human HT-12 beadarray.

ORGANISM(S): Homo sapiens  

SUBMITTER: Yu Chen   C D Allis  Ping Chi  Charles L Sawyers 

PROVIDER: E-GEOD-22433 | ArrayExpress | 2010-10-13



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Gastrointestinal stromal tumour (GIST) is the most common human sarcoma and is primarily defined by activating mutations in the KIT or PDGFRA receptor tyrosine kinases. KIT is highly expressed in interstitial cells of Cajal (ICCs)-the presumed cell of origin for GIST-as well as in haematopoietic stem cells, melanocytes, mast cells and germ cells. Yet, families harbouring germline activating KIT mutations and mice with knock-in Kit mutations almost exclusively develop ICC hyperplasia and GIST, su  ...[more]

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