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Gain of a region on 7p22.3, containing MAD1L1 , is the most frequent event in small‐cell lung cancer cell lines
Author(s) -
Coe Bradley P.,
Lee Eric H. L.,
Chi Bryan,
Girard Luc,
Minna John D.,
Gazdar Adi F.,
Lam Stephen,
MacAulay Calum,
Lam Wan L.
Publication year - 2006
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.20260
Subject(s) - comparative genomic hybridization , biology , loss of heterozygosity , gene dosage , copy number variation , cancer research , gene expression profiling , gene , genetics , computational biology , genome , gene expression , allele
Small‐cell lung cancer (SCLC) is a highly aggressive lung neoplasm, which accounts for 20% of yearly lung cancer cases. The lack of knowledge of the progenitor cell type for SCLC precludes the definition of a normal gene expression profile and has hampered the identification of gene expression changes, while the low resolution of conventional genomic screens such as comparative genomic hybridization (CGH) and loss of heterozygosity analysis limit our ability to fine‐map genetic alterations. The recent advent of whole genome tiling path array CGH enables profiling of segmental DNA copy number gains and losses at a resolution 100 times that of conventional methods. Here we report the analysis of 14 SCLC cell lines and six matched normal B‐lymphocyte lines. We detected 7p22.3 copy number gain in 13 of the 14 SCLC lines and 0 of the 6 matched normal lines. In 4 of the 14 cell lines, this gain is present as a 350 kbp gene specific copy number gain centered at MAD1L1 (the human homologue of the yeast gene MAD1 ). Fluorescence in situ hybridization validated the array CGH finding. Intriguingly, MAD1L1 has been implicated to have tumor‐suppressing functions. Our data suggest a more complex role for this gene, as MAD1L1 is the most frequent copy number gain in SCLC cell lines. © 2005 Wiley‐Liss, Inc.