TY - JOUR
T1 - Gene amplifications in osteosarcoma
T2 - CGH microarray analysis
AU - Atiye, Jassu
AU - Wolf, Maija
AU - Kaur, Sippy
AU - Monni, Outi
AU - Bohling, Tom
AU - Kivioja, Aarne
AU - Tas, Eva
AU - Serra, Massimo
AU - Tarkkanen, Maija
AU - Knuutila, Sakari
PY - 2005
Y1 - 2005
N2 - Little is known about the genomic alterations underlying osteosarcoma. We performed a genomewide high‐resolution gene copy number analysis of 22 osteosarcoma samples using comparative genomic hybridization on a cDNA microarray that contained cDNA clones of about 13,000 genes. Nineteen of the 22 cases had amplifications that on average spanned more than 1 Mb and contained more than 10 genes. Numerous regions of gain and loss were identified, and their boundaries were defined at high resolution. Novel amplicons were found at 14q11, 17q25, and 22q11–q13. Earlier‐known large amplified regions were detected at 12q11–q15, 8q24, 6p12–p13, and 17p11–p13 in 8, 6, 5, and 4 of the 22 samples, respectively. Amplification of 12q was observed more frequently (36% of the cases) than previously reported. Previously known small amplicons at 1p34–p36, 1q21, 19q13, and 21q22 were seen in at least three cases. Our results implicate TOM1L2 and CYP27B1 as having roles as novel targets for the 17p and 12q amplicons, respectively. Details (www.helsinki.fi/cmg) of the amplified genes in each amplicon provide valuable raw data for further in silico studies.
AB - Little is known about the genomic alterations underlying osteosarcoma. We performed a genomewide high‐resolution gene copy number analysis of 22 osteosarcoma samples using comparative genomic hybridization on a cDNA microarray that contained cDNA clones of about 13,000 genes. Nineteen of the 22 cases had amplifications that on average spanned more than 1 Mb and contained more than 10 genes. Numerous regions of gain and loss were identified, and their boundaries were defined at high resolution. Novel amplicons were found at 14q11, 17q25, and 22q11–q13. Earlier‐known large amplified regions were detected at 12q11–q15, 8q24, 6p12–p13, and 17p11–p13 in 8, 6, 5, and 4 of the 22 samples, respectively. Amplification of 12q was observed more frequently (36% of the cases) than previously reported. Previously known small amplicons at 1p34–p36, 1q21, 19q13, and 21q22 were seen in at least three cases. Our results implicate TOM1L2 and CYP27B1 as having roles as novel targets for the 17p and 12q amplicons, respectively. Details (www.helsinki.fi/cmg) of the amplified genes in each amplicon provide valuable raw data for further in silico studies.
U2 - 10.1002/gcc.20120
DO - 10.1002/gcc.20120
M3 - Article
SN - 1045-2257
VL - 42
SP - 158
EP - 163
JO - Genes, Chromosomes and Cancer
JF - Genes, Chromosomes and Cancer
IS - 2
ER -