Journal
NATURE COMMUNICATIONS
Volume 5, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/ncomms4518
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Funding
- 'CHEOPS'
- Deutsche Krebshilfe as part of the small-cell lung cancer genome-sequencing consortium [109679]
- EU-Framework program CURELUNG [HEALTH-F2-2010-258677]
- German federal state North Rhine Westphalia (NRW)
- European Union [005-1111-0025]
- Deutsche Forschungsgemeinschaft [TH1386/3-1, SFB832]
- German Ministry of Science and Education (BMBF) as part of the NGFNplus program [01GS08101]
- Deutsche Krebshilfe as part of the Oncology Centers of Excellence funding program
- Stand Up To Cancer-American Association for Cancer Research Innovative Research Grant [SU2C-AACR-IR60109]
- NIH K12 training grant [K12 CA9060625]
- Uniting Against Lung Cancer grant
- Damon Runyon Clinical Investigator Award
- AIRC and Istituto Toscano Tumori project [F13/16]
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Pulmonary carcinoids are rare neuroendocrine tumours of the lung. The molecular alterations underlying the pathogenesis of these tumours have not been systematically studied so far. Here we perform gene copy number analysis (n = 54), genome/exome (n = 44) and transcriptome (n = 69) sequencing of pulmonary carcinoids and observe frequent mutations in chromatin-remodelling genes. Covalent histone modifiers and subunits of the SWI/SNF complex are mutated in 40 and 22.2% of the cases, respectively, with MEN1, PSIP1 and ARID1A being recurrently affected. In contrast to small-cell lung cancer and large-cell neuroendocrine lung tumours, TP53 and RB1 mutations are rare events, suggesting that pulmonary carcinoids are not early progenitor lesions of the highly aggressive lung neuroendocrine tumours but arise through independent cellular mechanisms. These data also suggest that inactivation of chromatin-remodelling genes is sufficient to drive transformation in pulmonary carcinoids.
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