ArticleOncotarget2017
Genomic variations in paired normal controls for lung adenocarcinomas.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 17 citations in OpenAlex.
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- Expression status and prognostic value of the perilipin family of genes in breast cancer.American journal of translational research · 2021Article
- Systematic identification of CDC34 that functions to stabilize EGFR and promote lung carcinogenesis.EBioMedicine · 2020Article
- Tobacco, air pollution, environmental carcinogenesis, and thoughts on conquering strategies of lung cancer.Cancer biology & medicine · 2019Article
- Preferable background filtering for next-generation sequencing analysis in non-small cell lung cancer: pericarcinomatous tissues or peripheral blood lymphocytes?Cancer communications (London, England) · 2019Article
- The Aryl hydrocarbon receptor mediates tobacco-induced PD-L1 expression and is associated with response to immunotherapy.Nature communications · 2019Article
- Genomic variations in the counterpart normal controls of lung squamous cell carcinomas.Frontiers of medicine · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic genomic mutations in lung adenocarcinomas (LUADs) have been extensively dissected, but whether the counterpart normal lung tissues that are exposed to ambient air or tobacco smoke as the tumor tissues do, harbor genomic variations, remains unclear. Here, the genome of normal lung tissues and paired tumors of 11 patients with LUAD were sequenced, the genome sequences of counterpart normal controls (CNCs) and tumor tissues of 513 patients were downloaded from TCGA database and analyzed. In the initial screening, genomic alterations were identified in the "normal" lung tissues and verified by Sanger capillary sequencing. In CNCs of TCGA datasets, a mean of 0.2721 exonic variations/Mb and 5.2885 altered genes per sample were uncovered. The C:G→T:A transitions, a signature of tobacco carcinogen N-methyl-N-nitro-N-nitrosoguanidine, were the predominant nucleotide changes in CNCs. 16 genes had a variant rate of more than 2%, and CNC variations in
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