<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mahler-Araujo, M. B.</style></author><author><style face="normal" font="default" size="100%">Sanoudou, D.</style></author><author><style face="normal" font="default" size="100%">Tingby, O.</style></author><author><style face="normal" font="default" size="100%">Liu, L.</style></author><author><style face="normal" font="default" size="100%">Coleman, N.</style></author><author><style face="normal" font="default" size="100%">Ichimura, K.</style></author><author><style face="normal" font="default" size="100%">Collins, V. P.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Structural genomic abnormalities of chromosomes 9 and 18 in myxopapillary ependymomas</style></title><secondary-title><style face="normal" font="default" size="100%">J Neuropathol Exp NeurolJ Neuropathol Exp NeurolJ Neuropathol Exp Neurol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Journal of neuropathology and experimental neurology</style></alt-title><short-title><style face="normal" font="default" size="100%">Journal of neuropathology and experimental neurologyJournal of neuropathology and experimental neurology</style></short-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Central Nervous System Neoplasms/genetics/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 18/chemistry/*genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 9/chemistry/*genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Ependymoma/*genetics/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Microsatellite Repeats/genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms, Neuroepithelial/*genetics/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Peripheral Nervous System Neoplasms/genetics/pathology</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2003</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Sep</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">9</style></number><volume><style face="normal" font="default" size="100%">62</style></volume><pages><style face="normal" font="default" size="100%">927-35</style></pages><isbn><style face="normal" font="default" size="100%">0022-3069 (Print)0022-3069 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">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.</style></abstract><accession-num><style face="normal" font="default" size="100%">14533782</style></accession-num><notes><style face="normal" font="default" size="100%">Mahler-Araujo, Maria BetaniaSanoudou, DespinaTingby, OlaLiu, LuColeman, NicholasIchimura, KoichiCollins, Vincent PeterengComparative StudyResearch Support, Non-U.S. Gov'tEngland2003/10/10 05:00J Neuropathol Exp Neurol. 2003 Sep;62(9):927-35. doi: 10.1093/jnen/62.9.927.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Pathology, University of Cambridge, Cambridge, United Kingdom.</style></auth-address></record></records></xml>