OBJECT: Ependymomas are rare glial neoplasms; little is known about the molecular pathogenesis of this tumor entity. In a previous study the authors found multiple genomic imbalances in ependymomas resected in 20 adults and eight children, including loss of chromosomes 1p, 6, 16, 17, 19q, 20q, and 22q, as well as gain of chromosomes 4q, 5q, 7q, 9q, and 12q on comparative genomic hybridization. The aim of this study was to map in more detail the commonly affected regions in ependymomas. METHODS: A comprehensive allelotype analysis of 16 ependymomas was conducted using 384 microsatellite markers that span the 22 autosomes. Based on this high-resolution loss of heterozygosity analysis, multiple overlapping deletion regions were identified as follows: 6q25.2-27, 16p12-13.1, 16q22.3-24.1, 17q22-24, 19q12-13.2, 20q13.2-13.3, and 22q13.1-13.3. CONCLUSIONS: These data confirmed previous reports that loss of chromosomes 17 and 22 were common in ependymomas. Moreover, the authors were able to identify loss of chromosomes 13, 16, 19, and 20 as novel findings in ependymomas. It is believed that potential tumor suppressor genes that reside in these commonly deleted regions may contribute to the molecular tumorigenesis of ependymomas.
OBJECT: Ependymomas are rare glial neoplasms; little is known about the molecular pathogenesis of this tumor entity. In a previous study the authors found multiple genomic imbalances in ependymomas resected in 20 adults and eight children, including loss of chromosomes 1p, 6, 16, 17, 19q, 20q, and 22q, as well as gain of chromosomes 4q, 5q, 7q, 9q, and 12q on comparative genomic hybridization. The aim of this study was to map in more detail the commonly affected regions in ependymomas. METHODS: A comprehensive allelotype analysis of 16 ependymomas was conducted using 384 microsatellite markers that span the 22 autosomes. Based on this high-resolution loss of heterozygosity analysis, multiple overlapping deletion regions were identified as follows: 6q25.2-27, 16p12-13.1, 16q22.3-24.1, 17q22-24, 19q12-13.2, 20q13.2-13.3, and 22q13.1-13.3. CONCLUSIONS: These data confirmed previous reports that loss of chromosomes 17 and 22 were common in ependymomas. Moreover, the authors were able to identify loss of chromosomes 13, 16, 19, and 20 as novel findings in ependymomas. It is believed that potential tumor suppressor genes that reside in these commonly deleted regions may contribute to the molecular tumorigenesis of ependymomas.
Authors: Mandeep S Tamber; Krishan Bansal; Muh-Lii Liang; Todd G Mainprize; Bodour Salhia; Paul Northcott; Michael Taylor; James T Rutka Journal: Childs Nerv Syst Date: 2006-09-02 Impact factor: 1.475
Authors: Charles Teo; Peter Nakaji; Patricia Symons; Vivienne Tobias; Richard Cohn; Robert Smee Journal: Childs Nerv Syst Date: 2003-05-22 Impact factor: 1.475
Authors: Martin Gerard McCabe; Koichi Ichimura; Lu Liu; Karen Plant; L Magnus Bäcklund; Danita M Pearson; Vincent Peter Collins Journal: J Neuropathol Exp Neurol Date: 2006-06 Impact factor: 3.685