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Genomic variations in the counterpart normal controls of lung squamous cell carcinomas

Overview of attention for article published in Frontiers of Medicine, November 2017
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Title
Genomic variations in the counterpart normal controls of lung squamous cell carcinomas
Published in
Frontiers of Medicine, November 2017
DOI 10.1007/s11684-017-0580-1
Pubmed ID
Authors

Dalin Zhang, Liwei Qu, Bo Zhou, Guizhen Wang, Guangbiao Zhou

Abstract

Lung squamous cell carcinoma (LUSC) causes approximately 400 000 deaths each year worldwide. The occurrence of LUSC is attributed to exposure to cigarette smoke, which induces the development of numerous genomic abnormalities. However, few studies have investigated the genomic variations that occur only in normal tissues that have been similarly exposed to tobacco smoke as tumor tissues. In this study, we sequenced the whole genomes of three normal lung tissue samples and their paired adjacent squamous cell carcinomas.We then called genomic variations specific to the normal lung tissues through filtering the genomic sequence of the normal lung tissues against that of the paired tumors, the reference human genome, the dbSNP138 common germline variants, and the variations derived from sequencing artifacts. To expand these observations, the whole exome sequences of 478 counterpart normal controls (CNCs) and paired LUSCs of The Cancer Genome Atlas (TCGA) dataset were analyzed. Sixteen genomic variations were called in the three normal lung tissues. These variations were confirmed by Sanger capillary sequencing. A mean of 0.5661 exonic variations/Mb and 7.7887 altered genes per sample were identified in the CNC genome sequences of TCGA. In these CNCs, C:Gā†’T:A transitions, which are the genomic signatures of tobacco carcinogen N-methyl-N-nitro-N-nitrosoguanidine, were the predominant nucleotide changes. Twenty five genes in CNCs had a variation rate that exceeded 2%, including ARSD (18.62%), MUC4 (8.79%), and RBMX (7.11%). CNC variations in CTAGE5 and USP17L7 were associated with the poor prognosis of patients with LUSC. Our results uncovered previously unreported genomic variations in CNCs, rather than LUSCs, that may be involved in the development of LUSC.

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Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 18 100%

Demographic breakdown

Readers by professional status Count As %
Student > Doctoral Student 2 11%
Student > Bachelor 2 11%
Professor > Associate Professor 2 11%
Student > Master 1 6%
Lecturer > Senior Lecturer 1 6%
Other 2 11%
Unknown 8 44%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 22%
Agricultural and Biological Sciences 2 11%
Social Sciences 2 11%
Medicine and Dentistry 1 6%
Engineering 1 6%
Other 0 0%
Unknown 8 44%