Evidence map›Paper›PMID 22044695›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2012

Genetic variants associated with the risk of chronic obstructive pulmonary disease with and without lung cancer.

Mariza de Andrade, Yan Li, Randolph S Marks, Claude Deschamps, Paul D Scanlon, Curtis L Olswold, Ruoxiang Jiang, Stephen J Swensen, Zhifu Sun, Julie M Cunningham and 4 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 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

14 authors at 4 institutions in 2 countries.

Mariza de AndradeDivision of Epidemiology, Mayo Clinic, Rochester, MN 55905, USA.
Yan Li
Randolph S Marks
Claude Deschamps
Paul D Scanlon
Curtis L Olswold
Ruoxiang Jiang
Stephen J Swensen
Zhifu Sun
Julie M Cunningham
Jason A Wampfler
Andrew H Limper
David E Midthun
Ping Yang
Nanjing General Hospital of Nanjing Military Command · CNNanjing University · CNMayo Clinic · USNanjing Medical University · CN

Funding

ALPHA 1 AD CARRIERS AND LUNG CANCER RISKR01CA080127 · NCI · MAYO CLINIC ROCHESTER · PI YANG, PING · 2000 to 2009
$4.4M
Genetic Determinants of Lung Cancer SurvivalR01CA084354 · NCI · MAYO CLINIC ROCHESTER · PI YANG, PING · 2001 to 2012
$4.0M
DEVELOPMENT OF LUNG CANCER EPIDEMIOLOGY RESEARCHR03CA077118 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI YANG, PING · 1997 to 1998
–
NCI NIH HHS R01 CA080127NCI NIH HHS R01 CA084354NCI NIH HHS R01 CA80127NCI NIH HHS R01 CA84354NCI NIH HHS R03 CA077118NCI NIH HHS R03 CA77118
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a strong risk factor for lung cancer. Published studies about variations of genes encoding glutathione metabolism, DNA repair, and inflammatory response pathways in susceptibility to COPD were inconclusive. We evaluated 470 single-nucleotide polymorphisms (SNP) from 56 genes of these three pathways in 620 cases and 893 controls to identify susceptibility markers for COPD risk, using existing resources. We assessed SNP- and gene-level effects adjusting for sex, age, and smoking status. Differential genetic effects on disease risk with and without lung cancer were also assessed; cumulative risk models were established. Twenty-one SNPs were found to be significantly associated with risk of COPD (P < 0.01); gene-based analyses confirmed two genes (GCLC and GSS) and identified three additional genes (GSTO2, ERCC1, and RRM1). Carrying 12 high-risk alleles may increase risk by 2.7-fold; eight SNPs altered COPD risk without lung cancer by 3.1-fold and 4 SNPs altered the risk with lung cancer by 2.3-fold. Our findings indicate that multiple genetic variations in the three selected pathways contribute to COPD risk through GCLC, GSS, GSTO2, ERCC1, and RRM1 genes. Functional studies are needed to elucidate the mechanisms of these genes in the development of COPD, lung cancer, or both.

Indexed as

AdenocarcinomaAgedBiomarkers, TumorCase-Control StudiesFemaleGenotypeHumansLung NeoplasmsMalePolymorphism, Single NucleotidePulmonary Disease, Chronic ObstructiveRisk FactorsSmokingBiomarkers, Tumor

Identifiers

PMID22044695
PMCPMC3414259
OpenAlexW2133279306

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.