Dataset Information


Expression profiling data of CLB-GA neuroblastoma cells upon TAE-684, Crizotinib, X-396, LDK378, Trametinib, BEZ-235 and Vandetanib

ABSTRACT: Treatment of the CLB-GA cell line with complementary ALK, MEK, PI3K/mTOR or RET inhibitors (and DMSO (VWR) as control) was performed in duplicate for each drug using the GI50 concentrations (see further): 0.5ë_M Crizotinib (Pfizer/Sigma-Aldrich); 0.06ë_M X-396 (VWR); 0.2ë_M LDK378 (Hoelzel Biotech); 0.05uM Trametinib (SelleckChem); 0.5ë_M BEZ-235 (SelleckChem); 9.5ë_M Vandetanib (SelleckChem). Cells were collected at 6h following treatment and further profiled. The selected inhibitor concentrations were used based on determined GI50 values. For generation of gene expression time series following ALK inhibition, CLB-GA cells were treated with 0.3uM TAE-684 (and DMSO as control treatment) and RNA was harvested at 0 ÛÒ 10۪ ÛÒ 30۪ ÛÒ 60۪ ÛÒ 120۪ ÛÒ 240۪ ÛÒ 360۪ time points. Samples were labeled and hybridised to the Sureprint G3 human GE or G3 Mouse GE 8x60K microarrays (Agilent Technologies), according to the manufacturer۪s guidelines and starting from 200 ng of RNA.

ORGANISM(S): Homo sapiens  

SUBMITTER: Katleen De Preter  

PROVIDER: E-MTAB-3206 | ArrayExpress | 2015-05-04


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Upregulation of MAPK Negative Feedback Regulators and RET in Mutant ALK Neuroblastoma: Implications for Targeted Treatment.

Lambertz Irina I   Kumps Candy C   Claeys Shana S   Lindner Sven S   Beckers Anneleen A   Janssens Els E   Carter Daniel R DR   Cazes Alex A   Cheung Belamy B BB   De Mariano Marilena M   De Bondt An A   De Brouwer Sara S   Delattre Olivier O   Gibbons Jay J   Janoueix-Lerosey Isabelle I   Laureys Geneviève G   Liang Chris C   Marchall Glenn M GM   Porcu Michael M   Takita Junko J   Trujillo David Camacho DC   Van Den Wyngaert Ilse I   Van Roy Nadine N   Van Goethem Alan A   Van Maerken Tom T   Zabrocki Piotr P   Cools Jan J   Schulte Johannes H JH   Vialard Jorge J   Speleman Frank F   De Preter Katleen K  

Clinical cancer research : an official journal of the American Association for Cancer Research 20150324 14

Activating ALK mutations are present in almost 10% of primary neuroblastomas and mark patients for treatment with small-molecule ALK inhibitors in clinical trials. However, recent studies have shown that multiple mechanisms drive resistance to these molecular therapies. We anticipated that detailed mapping of the oncogenic ALK-driven signaling in neuroblastoma can aid to identify potential fragile nodes as additional targets for combination therapies.To achieve this goal, transcriptome profiling  ...[more]

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