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28 March 2024
 
  » pubmed » pmid17982442

 Article overview


Characterizing the cancer genome in lung adenocarcinoma
Barbara A Weir ; Michele S Woo ; Gad Getz ; Sven Perner ; Li Ding ; Rameen Beroukhim ; William M Lin ; Michael A Province ; Aldi Kraja ; Laura A Johnson ; Kinjal Shah ; Mitsuo Sato ; Roman K Thomas ; Justine A Barletta ; Ingrid B Borecki ; Stephen Broderick ; Andrew C Chang ; Derek Y Chiang ; Lucian R Chirieac ; Jeonghee Cho ; Yoshitaka Fujii ; Adi F Gazdar ; Thomas Giordano ; Heidi Greulich ; Megan Hanna ; Bruce E Johnson ; Mark G Kris ; Alex Lash ; Ling Lin ; Neal Lindeman ; Elaine R Mardis ; John D McPherson ; John D Minna ; Margaret B Morgan ; Mark Nadel ; Mark B Orringer ; John R Osborne ; Brad Ozenberger ; Alex H Ramos ; James Robinson ; Jack A Roth ; Valerie Rusch ; Hidefumi Sasaki ; Frances Shepherd ; Carrie Sougnez ; Margaret R Spitz ; Ming-Sound Tsao ; David Twomey ; Roel G W Verhaak ; George M Weinstock ; David A Wheeler ; Wendy Winckler ; Akihiko Yoshizawa ; Soyoung Yu ; Maureen F Zakowski ; Qunyuan Zhang ; David G Beer ; Ignacio I Wistuba ; Mark A Watson ; Levi A Garraway ; Marc Ladanyi ; William D Travis ; William Pao ; Mark A Rubin ; Stacey B Gabriel ; Richard A Gibbs ; Harold E Varmus ; Richard K Wilson ; Eric S Lander ; Matthew Meyerson ;
Date 4 Nov 2007
Journal Nature, (),
AbstractSomatic alterations in cellular DNA underlie almost all human cancers. The prospect of targeted therapies and the development of high-resolution, genome-wide approaches are now spurring systematic efforts to characterize cancer genomes. Here we report a large-scale project to characterize copy-number alterations in primary lung adenocarcinomas. By analysis of a large collection of tumours (n = 371) using dense single nucleotide polymorphism arrays, we identify a total of 57 significantly recurrent events. We find that 26 of 39 autosomal chromosome arms show consistent large-scale copy-number gain or loss, of which only a handful have been linked to a specific gene. We also identify 31 recurrent focal events, including 24 amplifications and 7 homozygous deletions. Only six of these focal events are currently associated with known mutations in lung carcinomas. The most common event, amplification of chromosome 14q13.3, is found in approximately 12% of samples. On the basis of genomic and functional analyses, we identify NKX2-1 (NK2 homeobox 1, also called TITF1), which lies in the minimal 14q13.3 amplification interval and encodes a lineage-specific transcription factor, as a novel candidate proto-oncogene involved in a significant fraction of lung adenocarcinomas. More generally, our results indicate that many of the genes that are involved in lung adenocarcinoma remain to be discovered.
Source PubMed, pmid17982442 doi: 10.1038/nature06358
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