CDKN2A/p16 in ependymomas

Sixteen cases of ependymoma were studied for CDKN2A/p16 inactivation by imm unohistochemistry using a p16 monoclonal antibody, by homozygous deletion ( HD) assay and 5'CpG promoter methylation assay (methylation-specific PCR). Three out of 16 cases were p16 immuno-negative: two corresponded to grade I I ependymomas and one to grade III. The latter ependymoma, characterized by a high Ki-67/MIB-1 LI, was the only one of the whole series to show CDKN2A HD. No promoter methylation was found in the two immuno-negative cases wit hout CDKN2A HD. Alternative mechanisms, such as point mutations or alterati ons in p16 post-translational regulation, may be responsible for p16 inacti vation. Since in our series just one out of eight anaplastic cases showed n egative immunostaining and CDKN2A HD, p16/CDKN2A inactivation may not play an important role in the malignant transformation of ependymomas. Amplification of CCND1 and CDK4, p27/Kip1 degradation and TP53 mutations we re previously studied by other authors and were demonstrated not to correla te with anaplasia. Up to date, molecular genetic studies have not been usef ul in recognizing the anaplastic variant in ependymomas.