ANAPLASTIC EPENDYMOMAS - CLINICAL-FEATURES AND TUMOR-SUPPRESSOR GENE P53 ANALYSIS

We analyzed seven cases of anaplastic ependymoma, focusing on neuro-im aging, histopathology, and mutations of the tumour suppressor gene p53 . Five of the seven tumours were supratentorial. All had both cystic a nd solid components, with fragment calcifications detectable on CT sca n. The solid parts of the tumours were imaged as heterogenous hypo- or iso-intense areas with moderate enhancement on T1-weighted magnetic r esonance images. Vascularity was not prominent on angiograms except fo r one case. Histologically, in addition to the WHO criteria, loss of t ypical cellular architecture, endothelial proliferation, and necrosis were commonly found. A mutation in Exon 5 of the tumour suppressor gen e p53 was detected in one anaplastic ependymoma out of five tumours (t wo benign and three anaplastic ependymomas) examined by PCR-SSPC analy sis of genomic DNA followed by direct sequencing. Anaplastic ependymom a typically presents as a calcified cystic tumour in the supratentoria l parenchyma or transependyma. Mutations of p53 deserve further invest igation to examine their possible role in the oncogenesis and malignan t transformation of ependymoma.