Evidence map›Paper›PMID 23056513›Full record

ArticlePloS one2012

Insights into pancreatic cancer etiology from pathway analysis of genome-wide association study data.

Peng Wei, Hongwei Tang, Donghui Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  11. Review
  12. NMolecular cancer · 2019
    Review
  13. Article
  14. Article
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  16. Article
  17. Article
  18. Aging · 2018
    Article
  19. Annals of hepato-biliary-pancreatic surgery · 2018
    Article
  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

3 authors at 2 institutions in 1 country.

Peng WeiDivision of Biostatistics and Human Genetics Center, School of Public Health, University of Texas Health Science Center, Houston, Texas, United States of America.
Hongwei Tang
Donghui Li
The University of Texas MD Anderson Cancer Center · USThe University of Texas Health Science Center at Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
U OF TEXAS HLTH SCI CTR HOUSTON CENTER FOR CLINICAL AND TRANSLATIONAL SCIENCESUL1RR024148 · NCRR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2006 to 2010
$27.9M
Molecular Epidemiology of Pancreatic CancerR01CA098380 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, DONGHUI · 2004 to 2008
$2.6M
Statistical Methods for Finding Missing HeritabilityR01HL106034 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI XIONG, MOMIAO · 2011 to 2014
$1.5M
Unified Statistical Methods for Sequence-Based Association StudiesR01GM104411 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI XIONG, MOMIAO · 2013 to 2016
$1.3M
NCI NIH HHS CA016672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA098380NCI NIH HHS R01 CA98380-05NCRR NIH HHS UL1 RR024148NHLBI NIH HHS R01 HL106034NHLBI NIH HHS R01HL106034-01NIGMS NIH HHS R01 GM104411
6 · The paper itself

Abstract

backgroundPancreatic cancer is the fourth leading cause of cancer death in the U.S. and the etiology of this highly lethal disease has not been well defined. To identify genetic susceptibility factors for pancreatic cancer, we conducted pathway analysis of genome-wide association study (GWAS) data in 3,141 pancreatic cancer patients and 3,367 controls with European ancestry.

methodsUsing the gene set ridge regression in association studies (GRASS) method, we analyzed 197 pathways identified from the Kyoto Encyclopedia of Genes and Genomes database. We used the logistic kernel machine (LKM) test to identify major contributing genes to each pathway. We conducted functional enrichment analysis of the most significant genes (P<0.01) using the Database for Annotation, Visualization, and Integrated Discovery (DAVID).

resultsTwo pathways were significantly associated with risk of pancreatic cancer after adjusting for multiple comparisons (P<0.00025) and in replication testing: neuroactive ligand-receptor interaction, (Ps<0.00002), and the olfactory transduction pathway (P = 0.0001). LKM test identified four genes that were significantly associated with risk of pancreatic cancer after Bonferroni correction (P<1×10(-5)): ABO, HNF1A, OR13C4, and SHH. Functional enrichment analysis using DAVID consistently found the G protein-coupled receptor signaling pathway (including both neuroactive ligand-receptor interaction and olfactory transduction pathways) to be the most significant pathway for pancreatic cancer risk in this study population.

conclusionThese novel findings provide new perspectives on genetic susceptibility to and molecular mechanisms of pancreatic cancer.

Indexed as

Genome-Wide Association StudyComputational BiologyGene Regulatory NetworksGenes, NeoplasmGenetic Predisposition to DiseaseHumansPancreatic NeoplasmsSignal Transduction

Identifiers

PMID23056513
PMCPMC3464266
OpenAlexW2112676113

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.