Evidence map›Paper›PMID 28056099›Full record

ArticlePloS one2017

Integrated Analysis of Genome-Wide Copy Number Alterations and Gene Expression Profiling of Lung Cancer in Xuanwei, China.

Yanliang Zhang, Qiuyue Xue, Guoqing Pan, Qing H Meng, Xiaoyu Tuo, Xuemei Cai, Zhenghui Chen, Ya Li, Tao Huang, Xincen Duan and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Yanliang ZhangDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Qiuyue XueDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Guoqing PanDepartment of Pathology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Qing H MengDepartment of Laboratory Medicine, University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Xiaoyu TuoDepartment of Pathology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Xuemei CaiDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Zhenghui ChenDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Ya LiDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Tao HuangDepartment of Thoracic Surgery, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
Xincen DuanDepartment of Biological Sciences, University of Wisconsin-Parkside, Somers, Wisconsin, United States of America.
Yong DuanDepartment of Clinical Laboratory, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan Province, the People's Republic of China.
First Affiliated Hospital of Kunming Medical University · CNKunming Medical University · CNThe University of Texas MD Anderson Cancer Center · USUniversity of Wisconsin–Parkside · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesLung cancer in Xuanwei (LCXW), China, is known throughout the world for its distinctive characteristics, but little is known about its pathogenesis. The purpose of this study was to screen potential novel "driver genes" in LCXW.

methodsGenome-wide DNA copy number alterations (CNAs) were detected by array-based comparative genomic hybridization and differentially expressed genes (DEGs) by gene expression microarrays in 8 paired LCXW and non-cancerous lung tissues. Candidate driver genes were screened by integrated analysis of CNAs and DEGs. The candidate genes were further validated by real-time quantitative polymerase chain reaction.

resultsLarge numbers of CNAs and DEGs were detected, respectively. Some of the most frequently occurring CNAs included gains at 5p15.33-p15.32, 5p15.1-p14.3, and 5p14.3-p14.2 and losses at 11q24.3, 21q21.1, 21q22.12-q22.13, and 21q22.2. Integrated analysis of CNAs and DEGs identified 24 candidate genes with frequent copy number gains and concordant upregulation, which were considered potential oncogenes, including CREB3L4, TRIP13, and CCNE2. In addition, the analysis identified 19 candidate genes with a negative association between copy number change and expression change, considered potential tumor suppressor genes, including AHRR, NKD2, and KLF10. One of the most studied oncogenes, MYC, may not play a carcinogenic role in LCXW.

conclusionsThis integrated analysis of CNAs and DEGs identified several potential novel LCXW-related genes, laying an important foundation for further research on the pathogenesis of LCXW and identification of novel biomarkers or therapeutic targets.

Indexed as

ChinaComparative Genomic HybridizationDNA Copy Number VariationsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiddle AgedOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain Reaction

Identifiers

PMID28056099
PMCPMC5215791
OpenAlexW2571199311

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.