Evidence map›Paper›PMID 26352532›Full record

ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2015

Lung Cancer Risk Prediction Using Common SNPs Located in GWAS-Identified Susceptibility Regions.

Joel L Weissfeld, Yan Lin, Hui-Min Lin, Brenda F Kurland, David O Wilson, Carl R Fuhrman, Arjun Pennathur, Marjorie Romkes, Tomoko Nukui, Jian-Min Yuan and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Predicting Drug Resistance inDiagnostics (Basel, Switzerland) · 2025
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  19. A Decade of GWAS Results in Lung Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Review
  20. 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

12 authors at 2 institutions in 1 country.

Joel L WeissfeldDepartments of *Epidemiology and †Biostatistics, Graduate School of Public Health, Pittsburgh, Pennsylvania; Departments of ‡Medicine, §Radiology, and ‖Cardiothoracic Surgery, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; and ¶Department of Pharmacology, School of Medicine, University of Minnesota, Minneapolis, Minnesota.
Yan Lin
Hui-Min Lin
Brenda F Kurland
David O Wilson
Carl R Fuhrman
Arjun Pennathur
Marjorie Romkes
Tomoko Nukui
Jian-Min Yuan
Jill M Siegfried
Brenda Diergaarde
University of Pittsburgh · USUniversity of Minnesota · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Vitamin D3 Modulation of Inflammation and Lung Cancer RiskP50CA090440 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DACIC, SANJA · 2001 to 2015
$34.6M
NCI NIH HHS P30 CA047904NCI NIH HHS P50 CA090440NCI NIH HHS P50 CA90440
6 · The paper itself

Abstract

introductionGenome-wide association studies (GWAS) have consistently identified specific lung cancer susceptibility regions. We evaluated the lung cancer-predictive performance of single-nucleotide polymorphisms (SNPs) in these regions.

methodsLung cancer cases (N = 778) and controls (N = 1166) were genotyped for 77 SNPs located in GWAS-identified lung cancer susceptibility regions. Variable selection and model development used stepwise logistic regression and decision-tree analyses. In a subset nested in the Pittsburgh Lung Screening Study, change in area under the receiver operator characteristic curve and net reclassification improvement were used to compare predictions made by risk factor models with and without genetic variables.

resultsVariable selection and model development kept two SNPs in each of three GWAS regions, rs2736100 and rs7727912 in 5p15.33, rs805297 and rs1802127 in 6p21.33, and rs8034191 and rs12440014 in 15q25.1. The ratio of cases to controls was three times higher among subjects with a high-risk genotype in every one as opposed to none of the three GWAS regions (odds ratio, 3.14; 95% confidence interval, 2.02-4.88; adjusted for sex, age, and pack-years). Adding a three-level classified count of GWAS regions with high-risk genotypes to an age and smoking risk factor-only model improved lung cancer prediction by a small amount: area under the receiver operator characteristic curve, 0.725 versus 0.717 (p = 0.056); overall net reclassification improvement was 0.052 across low-, intermediate-, and high- 6-year lung cancer risk categories (<3.0%, 3.0%-4.9%, ≥ 5.0%).

conclusionSpecifying genotypes for SNPs in three GWAS-identified susceptibility regions improved lung cancer prediction, but probably by an extent too small to affect disease control practice.

Indexed as

AgedAged, 80 and overFemaleGenome-Wide Association StudyHumansLung NeoplasmsMaleMiddle AgedPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID26352532
PMCPMC4636453
OpenAlexW1434731351

What OpenQuestion holds

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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.