Journal
CELL
Volume 150, Issue 6, Pages 1107-1120Publisher
CELL PRESS
DOI: 10.1016/j.cell.2012.08.029
Keywords
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Funding
- NCI [T32 CA9216]
- Canadian Institutes of Health
- American Cancer Society
- National Lung Cancer Partnership
- Dana-Farber/Harvard Cancer Center Lung Cancer SPORE [P50 CA090578]
- NIGMS [T32GM07753]
- German Ministry of Science and Education (BMBF) [01GS08100]
- Max Planck Society [M.I.F.A.NEUR8061]
- Deutsche Forschungsgemeinschaft (DFG) [SFB832 (TP6), TH1386/3-1]
- EU-Framework Programme CURELUNG [HEALTH-F2-2010-258677]
- American Association for Cancer Research [SU2C-AACR-IR60109]
- Behrens-Weise Foundation
- National Human Genome Research Institute
- National Cancer Institute
- Uniting Against Lung Cancer, the Lung Cancer Research Foundation
- American Lung Association
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Lung adenocarcinoma, the most common subtype of non-small cell lung cancer, is responsible for more than 500,000 deaths per year worldwide. Here, we report exome and genome sequences of 183 lung adenocarcinoma tumor/normal DNA pairs. These analyses revealed a mean exonic somatic mutation rate of 12.0 events/megabase and identified the majority of genes previously reported as significantly mutated in lung adenocarcinoma. In addition, we identified statistically recurrent somatic mutations in the splicing factor gene U2AF1 and truncating mutations affecting RBM10 and ARID1A. Analysis of nucleotide context-specific mutation signatures grouped the sample set into distinct clusters that correlated with smoking history and alterations of reported lung adenocarcinoma genes. Whole-genome sequence analysis revealed frequent structural rearrangements, including in-frame exonic alterations within EGFR and SIK2 kinases. The candidate genes identified in this study are attractive targets for biological characterization and therapeutic targeting of lung adenocarcinoma.
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