Genomic profiling identifies discrete deletions associated with translocations in glioblastoma multiforme. Mulholland, P. J., Fiegler, H., Mazzanti, C., Gorman, P., Sasieni, P., Adams, J., Jones, T. A., Babbage, J. W., Vatcheva, R., Ichimura, K., East, P., Poullikas, C., Collins, V. P., Carter, N. P., Tomlinson, I. P. M., & Sheer, D. Cell Cycle (Georgetown, Tex.), 5(7):783–791, April, 2006. doi abstract bibtex Glioblastoma multiforme is the most common tumor arising in the central nervous system. Patients with these tumors have limited treatment options and their disease is invariably fatal. Molecularly targeted agents offer the potential to improve patient treatment, however the use of these will require a fuller understanding of the genetic changes in these complex tumors. In this study, we identify copy number changes in a series of glioblastoma multiforme tumors and cell lines by applying high-resolution microarray comparative genomic hybridization. Molecular cytogenetic characterization of the cell lines revealed that copy number changes define translocation breakpoints. We focused on chromosome 6 and further characterized three regions of copy number change associated with translocations including a discrete deletion involving IGF2R, PARK2, PACRG and QKI and an unbalanced translocation involving POLH, GTPBP2 and PTPRZ1.
@article{mulholland_genomic_2006,
title = {Genomic profiling identifies discrete deletions associated with translocations in glioblastoma multiforme},
volume = {5},
issn = {1551-4005},
doi = {10.4161/cc.5.7.2631},
abstract = {Glioblastoma multiforme is the most common tumor arising in the central nervous system. Patients with these tumors have limited treatment options and their disease is invariably fatal. Molecularly targeted agents offer the potential to improve patient treatment, however the use of these will require a fuller understanding of the genetic changes in these complex tumors. In this study, we identify copy number changes in a series of glioblastoma multiforme tumors and cell lines by applying high-resolution microarray comparative genomic hybridization. Molecular cytogenetic characterization of the cell lines revealed that copy number changes define translocation breakpoints. We focused on chromosome 6 and further characterized three regions of copy number change associated with translocations including a discrete deletion involving IGF2R, PARK2, PACRG and QKI and an unbalanced translocation involving POLH, GTPBP2 and PTPRZ1.},
language = {eng},
number = {7},
journal = {Cell Cycle (Georgetown, Tex.)},
author = {Mulholland, Paul J. and Fiegler, Heike and Mazzanti, Chiara and Gorman, Patricia and Sasieni, Peter and Adams, Joanna and Jones, Tania A. and Babbage, Jane W. and Vatcheva, Radost and Ichimura, Koichi and East, Philip and Poullikas, Chrysanthos and Collins, V. Peter and Carter, Nigel P. and Tomlinson, Ian P. M. and Sheer, Denise},
month = apr,
year = {2006},
pmid = {16582634},
keywords = {Adult, Aged, Cell Line, Tumor, Chromosome Deletion, Chromosomes, Human, Pair 6, Chromosomes, Human, Pair 7, Cytogenetics, Female, Gene Dosage, Gene Expression, Gene Expression Profiling, Genome, Human, Genomics, Glioblastoma, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Nucleic Acid Hybridization, Translocation, Genetic},
pages = {783--791},
}
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Molecularly targeted agents offer the potential to improve patient treatment, however the use of these will require a fuller understanding of the genetic changes in these complex tumors. In this study, we identify copy number changes in a series of glioblastoma multiforme tumors and cell lines by applying high-resolution microarray comparative genomic hybridization. Molecular cytogenetic characterization of the cell lines revealed that copy number changes define translocation breakpoints. 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