Evidence map›Paper›PMID 25407004›Full record

ArticleEuropean journal of human genetics : EJHG2015

Duplicated copy of CHRNA7 increases risk and worsens prognosis of COPD and lung cancer.

Lei Yang, Xiaoxiao Lu, Fuman Qiu, Wenxiang Fang, Lisha Zhang, Dongsheng Huang, Chenli Xie, Nanshan Zhong, Pixin Ran, Yifeng Zhou and 1 more

Abstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Observational
  10. The etiologic origins for chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2019
    Review
  11. Article
  12. TwoInternational journal of chronic obstructive pulmonary disease · 2017
    Article
  13. Article
  14. Review
  15. Article
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.

Lei YangThe State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China.
Xiaoxiao Lu1] The State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China [2] Colby-Sawyer College, New London, NH, USA.
Fuman QiuThe State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China.
Wenxiang FangThe State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China.
Lisha ZhangThe State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China.
Dongsheng HuangDepartment of Respiratory Medicine, Guangzhou Chest Hospital, Guangzhou, China.
Chenli Xie1] The State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China [2] Dongguan Taiping People Hospital, Dongguan, China.
Nanshan ZhongThe First Affiliated Hospital, The State Key Lab of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Pixin RanThe First Affiliated Hospital, The State Key Lab of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Yifeng ZhouDepartment of Genetics, Medical College of Soochow University, Suzhou, China.
Jiachun LuThe State Key Lab of Respiratory Disease, The Institute for Chemical Carcinogenesis, Collaborative Innovation Center for Environmental Toxicity, Guangzhou Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent genome-wide association studies implicated that the nicotinic acetylcholine receptors (nAChRs) are common susceptible genes of two contextual diseases: chronic obstructive pulmonary disease (COPD) and lung cancer. We aimed to test whether the copy number variations (CNVs) in nAChRs have hereditary contributions to development of the two diseases. In two, two-stage, case-control studies of southern and eastern Chinese, a common CNV-3956 that duplicates the cholinergic receptor, nicotinic, α7 (CHRNA7) gene was genotyped in a total of 7880 subjects and its biological phenotype was assessed. The ≥4-copy of CNV-3956 increased COPD risk (≥4-copy vs 2/3-copy: OR=1.44, 95% CI=1.23-1.68) and caused poor lung function, and it similarly augmented risk (OR=1.49, 95% CI=1.29-1.73) and worsened prognosis (hazard ratio (HR)=1.25, 95% CI=1.07-1.45) of lung cancer. The ≥4-copy was estimated to account for 1.56% of COPD heritability and 1.87% of lung cancer heritability, respectively. Phenotypic analysis further showed that the ≥4-copy of CNV-3956 improved CHRNA7 expression in vivo and increased the carriers' smoking amount. The CNV-3956 of CHRNA7 contributed to increased risks and poor prognoses of both COPD and lung cancer, and this may be a genetic biomarker of the two diseases.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAsian PeopleCase-Control StudiesDNA Copy Number VariationsFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansLung NeoplasmsMalePrognosisPulmonary Disease, Chronic ObstructiveRisk Factorsalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, human

Identifiers

PMID25407004
PMCPMC4795111

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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.