CDKN2A , CDKN2B and p14 ARF are frequently and differentially methylated in ependymal tumours

Ependymal tumours are histologically and clinically varied lesions. Numerical abnormalities of chromosome 9 are frequently associated with these tumours. Nevertheless, the three important tumour suppressor genes located in this chromosome, CDKN2A , CDKN2B and p14 ARF , have not been reported to be commonly altered in them. We studied promoter methylation of these genes, an important mechanism associated with gene silencing in a series of 152 ependymal tumours of WHO grades I to III. Methylation status of the CDKN2A , CDKN2B and p14 ARF promoters was assessed by methylation‐specific polymerase chain reaction and the genetic results were correlated to clinicopathological features. We observed promoter methylation for CDKN2A in 21% (26/123) of tumours, for CDKN2B in 32% (23/71) and p14 ARF in 21% (23/108). For all three genes, posterior fossa ependymomas were less frequently methylated in paediatric patients than in adults. For CDKN2B , extracranial tumours were more frequently methylated than intracranial ones. For CDKN2B and p14 ARF , methylation was more frequent in low‐grade tumours; the reverse was observed for CDKN2A . CDKN2A , CDKN2B and p14 ARF promoters were methylated in 21–32% of the tumours. Frequencies of methylation varied  according  to clinicopathological features. This suggests a role for these genes in ependymoma tumorigenesis.