A combination of molecular cytogenetic analyses reveals complex genetic alterations in conventional renal cell carcinoma Export

@article{citeulike:3078615, abstract = {Here we report the complex pattern of genomic imbalances and rearrangements in a panel of 19 renal cell carcinoma cell lines detected with molecular cytogenetic analysis. Consistent heterogeneity in chromosome number was found, and most cell lines showed a near-triploid chromosome complement. Several cell lines showed deletions of the TP53 (alias p53), CDKN2A (alias p16), and VHL genes. Multiplex fluorescence in situ hybridization (M-FISH) analysis revealed chromosome 3 translocated to several other partners chromosomes, as well as breakage events commonly affecting chromosomes 1, 5, 8, 10, and 17. The most common abnormality detected with comparative genomic hybridization (CGH) was deletions of chromosome 3p, with loss of the RASSF1, FHIT, and p44S10 loci frequently involved. CGH gain of 5q showed overrepresentation of the EGR1 and CSF1R genes. Recurrent alterations to chromosome 7 included rearrangement of 7q11 and gains of the EGFR, TIF1, and RFC2 genes. Several lines exhibited rearrangement of 12q11\~{}q14 and overrepresentation of CDK4 and SAS loci. M-FISH revealed several other recurrent translocations, and CGH findings included loss of 9p, 14q, and 18q and gain of 8q, 12, and 20. Further genomic microarray changes included loss of MTAP, IGH@, HTR1B, and SMAD4 (previously MADH4) and gains of MYC and TOP1. An excellent correlation was observed between the genomic array and FISH data, demonstrating that this technique is effective and accurate. The aberrations detected here may reflect important pathways in renal cancer pathogenesis.}, author = {Strefford, Jon C. and Stasevich, Irina and Lane, Tim M. and Lu, Yong-Jie and Oliver, Tim and Young, Bryan D.}, citeulike-article-id = {3078615}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.cancergencyto.2004.09.020}, citeulike-linkout-1 = {http://www.sciencedirect.com/science/article/B6T53-4G1P192-3/2/b3974f2007df53fc8a6996a45ce93013}, doi = {10.1016/j.cancergencyto.2004.09.020}, journal = {Cancer Genetics and Cytogenetics}, keywords = {20q, top1}, month = {May}, number = {1}, pages = {1--9}, posted-at = {2008-08-03 18:03:29}, priority = {2}, title = {A combination of molecular cytogenetic analyses reveals complex genetic alterations in conventional renal cell carcinoma}, url = {http://dx.doi.org/10.1016/j.cancergencyto.2004.09.020}, volume = {159}, year = {2005} }

TY - JOUR ID - citeulike:3078615 L3 - citeulike-article-id:3078615 N2 - Here we report the complex pattern of genomic imbalances and rearrangements in a panel of 19 renal cell carcinoma cell lines detected with molecular cytogenetic analysis. Consistent heterogeneity in chromosome number was found, and most cell lines showed a near-triploid chromosome complement. Several cell lines showed deletions of the TP53 (alias p53), CDKN2A (alias p16), and VHL genes. Multiplex fluorescence in situ hybridization (M-FISH) analysis revealed chromosome 3 translocated to several other partners chromosomes, as well as breakage events commonly affecting chromosomes 1, 5, 8, 10, and 17. The most common abnormality detected with comparative genomic hybridization (CGH) was deletions of chromosome 3p, with loss of the RASSF1, FHIT, and p44S10 loci frequently involved. CGH gain of 5q showed overrepresentation of the EGR1 and CSF1R genes. Recurrent alterations to chromosome 7 included rearrangement of 7q11 and gains of the EGFR, TIF1, and RFC2 genes. Several lines exhibited rearrangement of 12q11~q14 and overrepresentation of CDK4 and SAS loci. M-FISH revealed several other recurrent translocations, and CGH findings included loss of 9p, 14q, and 18q and gain of 8q, 12, and 20. Further genomic microarray changes included loss of MTAP, IGH@, HTR1B, and SMAD4 (previously MADH4) and gains of MYC and TOP1. An excellent correlation was observed between the genomic array and FISH data, demonstrating that this technique is effective and accurate. The aberrations detected here may reflect important pathways in renal cancer pathogenesis. IS - 1 JF - Cancer Genetics and Cytogenetics EP - 9 TI - A combination of molecular cytogenetic analyses reveals complex genetic alterations in conventional renal cell carcinoma VL - 159 SP - 1 KW - 20q KW - top1 AU - Strefford, Jon AU - Stasevich, Irina AU - Lane, Tim AU - Lu, Yong-Jie AU - Oliver, Tim AU - Young, Bryan PY - 2005/05// UR - http://dx.doi.org/10.1016/j.cancergencyto.2004.09.020 ER -