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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 year - 2003
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.0305-1846.2003.00505.x
Subject(s) - cdkn2b , cdkn2a , methylation , biology , carcinogenesis , cancer research , ependymoma , microbiology and biotechnology , gene , pathology , medicine , genetics
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.