Epigenetic alterations, including methylation, have been shown to be an 
important mechanism of gene silencing in cancer. Ependymoma has been well 
characterized at the DNA copy number and mRNA expression levels. However little 
is known about DNA methylation changes. To gain a more global view of the 
methylation profile of ependymoma we conducted an array-based analysis. Our data 
demonstrated tumors to segregate according to their location in the CNS, which 
was associated with a difference in the global level of methylation. 
Supratentorial and spinal tumors displayed significantly more hypermethylated 
genes than posterior fossa tumors, similar to the 'CpG island methylator 
phenotype' (CIMP) identified in glioma and colon carcinoma. This hypermethylated 
profile was associated with an increase in expression of genes encoding for 
proteins involved in methylating DNA, suggesting an underlying mechanism. An 
integrated analysis of methylation and mRNA expression array data allowed us to 
identify methylation-induced expression changes. Most notably genes involved in 
the control of cell growth and death and the immune system were identified, 
including members of the JNK pathway and PPARG. In conclusion, we have generated 
a global view of the methylation profile of ependymoma. The data suggests 
epigenetic silencing of tumor suppressor genes is an important mechanism in the 
pathogenesis of supratentorial and spinal, but not posterior fossa ependymomas. 
Hypermethylation correlated with a decrease in expression of a number of tumor 
suppressor genes and pathways that could be playing an important role in tumor 
pathogenesis.