Clinical utility of fluorescence in situ hybridization (FISH) in nonbrainstem glioblastomas of childhood

Department of Neuropathology, NN Burdenko Neurosurgical Institute, Moscow, Russia.
Modern Pathology (Impact Factor: 6.19). 10/2005; 18(9):1258-63. DOI: 10.1038/modpathol.3800415
Source: PubMed


Astrocytic gliomas are the most common pediatric brain tumors; however, nonbrainstem glioblastomas are extremely rare compared with their adult counterparts. Little information is available on the clinical significance of various molecular markers in pediatric grade IV astrocytomas. The current study was focused on the molecular analysis and clinico-pathological correlations in a set of 44 tumor samples obtained from pediatric patients with nonbrainstem glioblastomas. Fluorescence in situ hybridization (FISH) with a set of 10 commercial chromosome probes (1p36, 1q25, centromere (CEP)7, EGFR, CEP9, 9p21/p16, CEP10, 10q23/PTEN, 19p13, and 19q13) was performed. Disclosed molecular abnormalities, in descending order of frequency, included polysomy 7 (72%), loss of 10q23 (61%), loss of 9p21 (52%), loss of 1p36 (41%), gain of 1q25 (25%), polysomy 9 (16%), EGFR amplification (9%), loss of 19q13 (5%), polysomy 19 (5%), and codeletion 1p36/19q13 (2%). The overall survival time was markedly shorter only for those patients whose lesions harbored deletion of 10q23/PTEN locus (log-rank test; P=0.00007). By multivariate analysis, only loss of 10q23 locus reached an independent level of prognostic value (hazard ratio=2.88; P=0.01). There were no significant differences in patient survival for other molecular abnormalities. In conclusion, a FISH analysis of 10q23 dosage should be recommended as an ancillary laboratory method that allows further clinical subdivision of pediatric glioblastomas.

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Available from: Andrey Korshunov, Mar 25, 2014
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    • "Based on hybridisation in 10 control cores (data not shown), hemizygous deletion of PTEN were defined as 420% (mean þ 3 s.d. in non-neoplastic controls) of tumour nuclei containing one PTEN locus signal and by the presence of CEP 10 signals. Homozygous deletion of PTEN was exhibited by the simultaneous lack of the both PTEN locus signals and by the presence of control signals (Mezzelani et al, 1999; Kawai et al, 2004; Korshunov et al, 2005; Ventura et al, 2006) in 430% of cells (Korshunov et al, 2005). "
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