Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences. vol:41 issue:4 pages:191-5
Fluorescence in situ hybridisation (FISH) analysis using total chromosome 22 painting and locus specific 22q11.2 (bcr locus) probes was performed on sections from archival paraffin-embedded tumours obtained from 28 patients diagnosed with either ependymoma, WHO grade 11 (18 cases) or anaplastic ependymoma, WHO grade 111 (10 cases). The Ki-67 labelling index (LI) analysis was carried out in parallel to estimate the tumours' proliferative potential. Loss of chromosome 22 was revealed in eleven (39%) ependymomas, seven (39%) WHO grade II and four (40%) anaplastic variants. Concurrent cytogenetic analysis was performed on 11 tumours to confirm the loss of chromosome 22 in four cases; clones with a loss of chromosome 22, which was identified by FISH, were not detected by standard cytogenetics in two samples. The loss of chromosome 22 was restricted either to the tumours' site or to sex or age of the patients studied. The Ki-67 LI ranged from 0.1 to 32.0% (mean 4.3%). Low-grade tumours significantly showed a lower mean Ki-67 LI than those classified as anaplastic tumours (3.1% and 6.4%, respectively). Additionally, the mean Ki-67 LI for ependymomas with a loss of chromosome 22 was significantly lower than that for tumours with chromosome 22 disomy (1.6% and 6.0%, respectively, p = 0.05), indicating that loss of chromosome 22 may be associated with the subset of ependymomas characterised by low proliferative capacities.