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Central neurocytomas are genetically distinct from oligodendrogliomas and neuroblastomas
Author(s) -
Tong C Y K,
Ng HK,
Pang J C S,
Hu J,
Hui A B Y,
Poon WS
Publication year - 2000
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.2000.00977.x
Subject(s) - loss of heterozygosity , biology , central neurocytoma , fluorescence in situ hybridization , oligodendroglioma , gene duplication , carcinogenesis , pathology , chromosome , oligodendroglial tumor , allele , gene , cancer research , genetics , glioma , astrocytoma , medicine , radiology , magnetic resonance imaging
Aims Central neurocytoma is a rare central nervous system tumour typically found in the lateral ventricles and at the septum pellucidum. Histologically, it resembles oligodendrogliomas and yet ultrastructurally, it shows neuronal differentiation. Its molecular oncogenesis is not known. The aim of this study was to examine whether major genetic events found in oligodendrogliomas and neuronal tumours, namely allelic deletions of chromosomes 1p and 19q and N‐myc amplification, can be found in central neurocytomas. As there was one report describing gain of chromosome 7 in central neurocytomas, we also examined epidermal growth factor receptor ( EGFR ) amplification, as the EGFR gene is located at chromosome 7p. Methods and results Nine central neurocytomas and matched blood samples were examined for loss of heterozygosity (LOH) of 1p and 19q13.2–13.4 with 23 finely mapped microsatellite markers. N‐myc amplification was studied by fluorescence in‐situ hybridization using paraffin‐embedded sections. EGFR amplification was tested for by differential PCR. Six of nine (67%) tumours showed LOH at one or more loci at 1p and 5/9 (56%) of cases showed LOH at 19q. However, common regions of deletion cannot be identified. The majority of informative markers are retained at 1p (84%) and 19q (86%). Only one tumour showed amplification of N‐myc and none of the cases showed amplification of EGFR . Conclusion Central neurocytomas are genetically distinct from oligodendrogliomas, and chromosomes 1p and 19q probably do not play an important role in their pathogenesis. N‐myc and EGFR amplification are rare.

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