Structural Genomic Abnormalities of Chromosomes 9 and 18 in Myxopapillary Ependymomas

Myxopapillary ependymomas (MPEs) are low-grade neuroepithelial tumors typically occurring in the conus - cauda equina - filum terminale region. Limited molecular and cytogenetic analysis of MPEs has not demonstrated consistent abnormalities. In an attempt to clarify the chromosomal status of these t...

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Bibliographic Details
Published in:Journal of neuropathology and experimental neurology 2003-09, Vol.62 (9), p.927-935
Main Authors: MAHLER-ARAUJO, MARIA BETANIA, SANOUDOU, DESPINA, TINGBY, OLA, LIU, LU, COLEMAN, NICHOLAS, ICHIMURA, KOICHI, COLLINS, VINCENT PETER
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Biological and medical sciences
Central Nervous System Neoplasms - genetics
Central Nervous System Neoplasms - pathology
Chromosomes, Human, Pair 18 - chemistry
Chromosomes, Human, Pair 18 - genetics
Chromosomes, Human, Pair 9 - chemistry
Chromosomes, Human, Pair 9 - genetics
Conus
Ependymoma - genetics
Ependymoma - pathology
Female
Humans
Male
Medical sciences
Microsatellite Repeats - genetics
Middle Aged
Neoplasms, Neuroepithelial - genetics
Neoplasms, Neuroepithelial - pathology
Neurology
Peripheral Nervous System Neoplasms - genetics
Peripheral Nervous System Neoplasms - pathology
Tumors of the nervous system. Phacomatoses
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Summary:Myxopapillary ependymomas (MPEs) are low-grade neuroepithelial tumors typically occurring in the conus - cauda equina - filum terminale region. Limited molecular and cytogenetic analysis of MPEs has not demonstrated consistent abnormalities. In an attempt to clarify the chromosomal status of these tumors and identify commonly aberrant regions in the genome we have combined 3 molecular/cyto/genetic methods to study 17 MPEs. Comparative genomic hybridization of 7/17 tumors identified concurrent gain on chromosomes 9 and 18 as the most frequent finding. The majority of the 17 tumors were also studied using microsatellite analysis with marker spanning the whole chromosomes 9 and 18 and interphase-FISH with centromeric probes for both chromosomes. Our combined results were consistent with concurrent gain in both chromosomes 9 and 18 in 11/17 cases, gain of either chromosome 9 or 18 and imbalance in the other chromosome in 3/17 tumors and allelic imbalances of chromosomes 9 or 18 in 3/17 and 1/17 tumors, respectively. Other abnormalities observed included gain of chromosomes 3, 4, 7, 8, 11, 13, 17q, 20, and X and loss of chromosomes 10 and 22. Our findings represent some steps towards understanding the molecular mechanisms involved in the development of MPE.
ISSN:0022-3069
1554-6578
DOI:10.1093/jnen/62.9.927