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Homozygous Deletions and Chromosome Amplifications in Human Lung Carcinomas Revealed by Single Nucleotide Polymorphism Array Analysis

Departments of ¹ Medical Oncology and ² Biostatistical Sciences, and ³ Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute; Departments of ⁴ Pathology and ⁵ Medicine, Harvard Medical School; Departments of ⁶ Biostatistics and ⁷ Environmental Health, Harvard School of Public Health, Boston, Massachusetts; Departments of ⁸ Pathology and ⁹ Medicine, and ¹⁰ Division of Thoracic Surgery, Brigham and Women's Hospital, Boston, Massachusetts; ¹¹ Department of Respiratory Medicine, Yokohama Municipal Citizen's Hospital, Yokohama, Japan; ¹² Hamon Center for Therapeutic Oncology Research; ¹³ Departments of Internal Medicine and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas; and ¹⁴ Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts

Requests for reprints: Matthew Meyerson, Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115. Phone: 617-632-4768; Fax: 617-632-5998; E-mail: matthew_meyerson{at}dfci.harvard.edu.

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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