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

Xiaojun Zhao; Barbara A. Weir; Thomas LaFramboise; Ming Lin; Rameen Beroukhim; Levi Garraway; Javad Beheshti; Jeffrey C. Lee; Katsuhiko Naoki; William G. Richards; David Sugarbaker; Fei Chen; Mark A. Rubin; Pasi A. Jänne; Luc Girard; John Minna; David Christiani; Cheng Li; William R. Sellers; Matthew Meyerson

doi:10.1158/0008-5472.CAN-04-4603

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

Xiaojun Zhao, Barbara A. Weir, Thomas LaFramboise, Ming Lin, Rameen Beroukhim, Levi Garraway, Javad Beheshti, Jeffrey C. Lee, Katsuhiko Naoki, William G. Richards, David Sugarbaker, Fei Chen, Mark A. Rubin, Pasi A. Jänne, Luc Girard, John Minna, David Christiani, Cheng Li, William R. Sellers, Matthew Meyerson

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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 ∼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.

Original language	English (US)
Pages (from-to)	5561-5570
Number of pages	10
Journal	Cancer research
Volume	65
Issue number	13
DOIs	https://doi.org/10.1158/0008-5472.CAN-04-4603
State	Published - Jul 1 2005

ASJC Scopus subject areas

Oncology
Cancer Research

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Zhao, X., Weir, B. A., LaFramboise, T., Lin, M., Beroukhim, R., Garraway, L., Beheshti, J., Lee, J. C., Naoki, K., Richards, W. G., Sugarbaker, D., Chen, F., Rubin, M. A., Jänne, P. A., Girard, L., Minna, J., Christiani, D., Li, C., Sellers, W. R., & Meyerson, M. (2005). Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis. Cancer research, 65(13), 5561-5570. https://doi.org/10.1158/0008-5472.CAN-04-4603

Zhao, 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 2005, 'Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis', Cancer research, vol. 65, no. 13, pp. 5561-5570. https://doi.org/10.1158/0008-5472.CAN-04-4603

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title = "Homozygous deletions and chromosome amplifications in human lung carcinomas revealed by single nucleotide polymorphism array analysis",

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 ∼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.",

author = "Xiaojun Zhao and Weir, {Barbara A.} and Thomas LaFramboise and Ming Lin and Rameen Beroukhim and Levi Garraway and Javad Beheshti and Lee, {Jeffrey C.} and Katsuhiko Naoki and Richards, {William G.} and David Sugarbaker and Fei Chen and Rubin, {Mark A.} and J{\"a}nne, {Pasi A.} and Luc Girard and John Minna and David Christiani and Cheng Li and Sellers, {William R.} and Matthew Meyerson",

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doi = "10.1158/0008-5472.CAN-04-4603",

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AU - Zhao, Xiaojun

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AU - LaFramboise, Thomas

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AU - Beroukhim, Rameen

AU - Garraway, Levi

AU - Beheshti, Javad

AU - Lee, Jeffrey C.

AU - Naoki, Katsuhiko

AU - Richards, William G.

AU - Sugarbaker, David

AU - Chen, Fei

AU - Rubin, Mark A.

AU - Jänne, Pasi A.

AU - Girard, Luc

AU - Minna, John

AU - Christiani, David

AU - Li, Cheng

AU - Sellers, William R.

AU - Meyerson, Matthew

PY - 2005/7/1

Y1 - 2005/7/1

N2 - 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 ∼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.

AB - 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 ∼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.

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

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