Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis.

TitleHomozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis.
Publication TypeJournal Article
Year of Publication2005
AuthorsZhao X, Weir BA, LaFramboise T, Lin M, Beroukhim R, Garraway L, Beheshti J, Lee JC, Naoki K, Richards WG, Sugarbaker D, Chen F, Rubin MA, Jänne PA, Girard L, Minna J, Christiani D, Li C, Sellers WR, Meyerson M
JournalCancer Res
Volume65
Issue13
Pagination5561-70
Date Published2005 Jul 1
ISSN0008-5472
KeywordsCarcinoma, Non-Small-Cell Lung, Carcinoma, Small Cell, Cell Line, Tumor, Chromosome Aberrations, Chromosome Deletion, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, Cyclin-Dependent Kinases, DNA, Neoplasm, Gene Amplification, Gene Dosage, Genome, Human, Humans, Lung Neoplasms, Polymorphism, Single Nucleotide, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Receptor, Epidermal Growth Factor
Abstract

Genome-wide copy number changes were analyzed in 70 primary human lung carcinoma specimens and 31 cell lines derived from human lung carcinomas, with high-density arrays representing approximately 115,000 single nucleotide polymorphism loci. In addition to previously characterized loci, two regions of homozygous deletion were found, one near the PTPRD locus on chromosome segment 9p23 in four samples representing both small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC) and the second on chromosome segment 3q25 in one sample each of NSCLC and SCLC. High-level amplifications were identified within chromosome segment 8q12-13 in two SCLC specimens, 12p11 in two NSCLC specimens and 22q11 in four NSCLC specimens. Systematic copy number analysis of tyrosine kinase genes identified high-level amplification of EGFR in three NSCLC specimens, FGFR1 in two specimens and ERBB2 and MET in one specimen each. EGFR amplification was shown to be independent of kinase domain mutational status.

DOI10.1158/0008-5472.CAN-04-4603
Alternate JournalCancer Res.
PubMed ID15994928
Grant List2P30 CA06516-39 / CA / NCI NIH HHS / United States
P50CA70907 / CA / NCI NIH HHS / United States
T32 CA009172 / CA / NCI NIH HHS / United States