ArrayExpress Uploaderarrayexpress_sidhumannoneIN3008noneIN30085-Aza-dC (5 �mol/L)IN30085-Aza-dC (5 �mol/L)IN3008noneIN1638noneIN16385-Aza-dC (5 �mol/L)IN16385-Aza-dC (5 �mol/L)IN1638noneIN1594noneIN15945-Aza-dC (5 �mol/L)IN15945-Aza-dC (5 �mol/L)IN1594220104Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer,...E-GEOD-45437/profile/8773/arrayexpressuploader212braincancercellgenomeDec.12, 2014FalseE-GEOD-45437_A-AFFY-44expression-data-from-paediatric-ependymoma-short-tExpression data from paediatric ependymoma short-term cell culturesJul.11, 2014Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours. To identify targets of epigenetic silencing mediated by CpG island methylation in paediatric ependymoma, we used a pharmacological unmasking approach through treatment with the demethylating agent 5-Aza-2’-deoxycytidine followed by global expression microarray analysis. Three short-term ependymoma cell cultures were used for whole genome expression analysis following treatment with the demethylating agent 5-Aza-dC (5 µmol/L) or mock-treated with DMSO (≤0.1% v/v) for 96-hrs.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-45437http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-45437/samples/