High-resolution analysis of gene copy number alterations in human prostate cancer using CGH on cDNA microarrays: impact of copy number on gene expression. Export

@article{citeulike:933924, abstract = {Identification of target genes for genetic rearrangements in prostate cancer and the impact of copy number changes on gene expression are currently not well understood. Here, we applied high-resolution comparative genomic hybridization (CGH) on cDNA microarrays for analysis of prostate cancer cell lines. CGH microarrays identified most of the alterations detected by classic chromosomal CGH, as well as a number of previously unreported alterations. Specific recurrent regions of gain (28) and loss (18) were found, and their boundaries defined with sub-megabasepair accuracy. The most common changes included copy number decreases at 13q, and gains at 1q and 5p. Refined mapping identified several sites, such as at 13q (33-44, 49-51, and 74-76 Mbp from the p-telomere), which matched with minimal regions of loss seen in extensive loss of heterozygosity mapping studies of large numbers of tumors. Previously unreported recurrent changes were found at 2p, 2q, 3p, and 17q (losses), and at 3q, 5p, and 6p (gains). Integration of genomic and transcriptomic data revealed the role of individual candidate target genes for genomic alterations as well as a highly significant (P <.0001) overall association between copy number levels and the percentage of differentially expressed genes. Across the genome, the overall impact of copy number on gene expression levels was, to a large extent, attributable to low-level gains and losses of copy number, corresponding to common deletions and gains of often large chromosomal regions.}, address = {Medical Biotechnology, VTT Technical Research Centre of Finland and University of Turku, Turku FIN-20520, Finland.}, author = {Wolf, M. and Mousses, S. and Hautaniemi, S. and Karhu, R. and Huusko, P. and Allinen, M. and Elkahloun, A. and Monni, O. and Chen, Y. and Kallioniemi, A. and Kallioniemi, O. P.}, citeulike-article-id = {933924}, citeulike-linkout-0 = {http://dx.doi.org/10.1593/neo.3439}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15153336}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15153336}, doi = {10.1593/neo.3439}, issn = {1522-8002}, journal = {Neoplasia}, keywords = {cancer, cgh, cnv, prostate}, number = {3}, pages = {240--247}, posted-at = {2009-03-16 17:24:03}, priority = {2}, title = {High-resolution analysis of gene copy number alterations in human prostate cancer using CGH on cDNA microarrays: impact of copy number on gene expression.}, url = {http://dx.doi.org/10.1593/neo.3439}, volume = {6}, year = {2004} }

TY - JOUR ID - citeulike:933924 L3 - citeulike-article-id:933924 N2 - Identification of target genes for genetic rearrangements in prostate cancer and the impact of copy number changes on gene expression are currently not well understood. Here, we applied high-resolution comparative genomic hybridization (CGH) on cDNA microarrays for analysis of prostate cancer cell lines. CGH microarrays identified most of the alterations detected by classic chromosomal CGH, as well as a number of previously unreported alterations. Specific recurrent regions of gain (28) and loss (18) were found, and their boundaries defined with sub-megabasepair accuracy. The most common changes included copy number decreases at 13q, and gains at 1q and 5p. Refined mapping identified several sites, such as at 13q (33-44, 49-51, and 74-76 Mbp from the p-telomere), which matched with minimal regions of loss seen in extensive loss of heterozygosity mapping studies of large numbers of tumors. Previously unreported recurrent changes were found at 2p, 2q, 3p, and 17q (losses), and at 3q, 5p, and 6p (gains). Integration of genomic and transcriptomic data revealed the role of individual candidate target genes for genomic alterations as well as a highly significant (P <.0001) overall association between copy number levels and the percentage of differentially expressed genes. Across the genome, the overall impact of copy number on gene expression levels was, to a large extent, attributable to low-level gains and losses of copy number, corresponding to common deletions and gains of often large chromosomal regions. IS - 3 JF - Neoplasia SN - 1522-8002 AD - Medical Biotechnology, VTT Technical Research Centre of Finland and University of Turku, Turku FIN-20520, Finland. EP - 247 TI - High-resolution analysis of gene copy number alterations in human prostate cancer using CGH on cDNA microarrays: impact of copy number on gene expression. VL - 6 SP - 240 KW - cancer KW - cgh KW - cnv KW - prostate AU - Wolf, M AU - Mousses, S AU - Hautaniemi, S AU - Karhu, R AU - Huusko, P AU - Allinen, M AU - Elkahloun, A AU - Monni, O AU - Chen, Y AU - Kallioniemi, A AU - Kallioniemi, OP PY - 2004///n UR - http://dx.doi.org/10.1593/neo.3439 ER -