Dataset Information


MRNA expression profiles of SK-N-AS neuroblastoma cells with induced ALK-wt, ALK-F1174L or ALK-R1275Q

ABSTRACT: Establishment of inducible SK-N-AS ALKwt, ALKF1174L and ALKR1275Q cell lines Human neuroblastoma SK-N-AS cells were electroporated with pcDNA6/TR (Invitrogen) using the Neonå¨ Transfection System (Life Techologies). Single cell clones were generated using blasticidin (7.5åµg/ml) and limited dilution. Using a TetR antibody (Clonetech), the clone with the highest TetR expression was selected (named SK-N-AS-TR) and used for the transfection with pT-REx-DEST30-ALK, ALKF1174L or ALKR1275Q. After transfection of SK-N-AS-TR with the ALK variants, single cell clones were raised using geneticin (500 åµg/ml) and limited dilution, while blasticidin treatment was continued as described above. Total RNA of (treated) cell lines, transgenic mice tumors and ganglia was isolated using the miRNeasy kit (Qiagen) according to the manufacturer۪s instructions, including on-column DNase treatment. 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-3207 | 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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