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Premium CDKN2A , CDKN2B and p14 ARF are frequently and differentially methylated in ependymal tumours
Author(s)
Rousseau E.,
Ruchoux M.M.,
Scaravilli F.,
Chapon F.,
Vinchon M.,
De Smet C.,
Godfraind C.,
Vikkula M.
Publication year2003
Publication title
neuropathology and applied neurobiology
Resource typeJournals
PublisherBlackwell Science Ltd
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.
Subject(s)biology , cancer research , carcinogenesis , cdkn2a , cdkn2b , ependymoma , gene , genetics , medicine , methylation , microbiology and biotechnology , pathology
Language(s)English
SCImago Journal Rank2.538
H-Index95
eISSN1365-2990
pISSN0305-1846
DOI10.1046/j.0305-1846.2003.00505.x

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