Evidence map›Paper›PMID 32367578›Full record

ArticleMolecular carcinogenesis2020

Genetic variants of the peroxisome proliferator-activated receptor (PPAR) signaling pathway genes and risk of pancreatic cancer.

Xiaowen Liu, Danwen Qian, Hongliang Liu, James L Abbruzzese, Sheng Luo, Kyle M Walsh, Qingyi Wei

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 20 citations in OpenAlex.

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  6. Genetic Variants ofJournal of hepatocellular carcinoma · 2025
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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

7 authors at 2 institutions in 2 countries.

Xiaowen LiuDepartment of Gastric Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Danwen QianDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Hongliang LiuDuke Cancer Institute, Duke University Medical Center, Durham, North Carolina.
James L AbbruzzeseDuke Cancer Institute, Duke University Medical Center, Durham, North Carolina.
Sheng LuoDepartment of Biostatistics and Bioinformatics, Duke University School of Medicine, Durham, North Carolina.
Kyle M WalshDuke Cancer Institute, Duke University Medical Center, Durham, North Carolina.
Qingyi WeiDuke Cancer Institute, Duke University Medical Center, Durham, North Carolina.ORCID 0000-0002-3845-9445
Duke University · USShanghai Medical College of Fudan University · CN

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI Laura Fish · 1985 to 2026
$174.8M
Validation and Fine-Scale Mapping of Pancreatic Cancer Susceptibility Loci (Study)R01CA154823 · NCI · JOHNS HOPKINS UNIVERSITY · PI KLEIN, ALISON P · 2011 to 2020
$5.7M
Cohort Study of Biochemical and Genetic Risk Factors for Pancreatic CancerK07CA140790 · NCI · DANA-FARBER CANCER INST · PI WOLPIN, BRIAN MATTHEW · 2009 to 2013
$890k
CCR NIH HHS HHSN261200800001CHoward Hughes Medical InstituteNCI NIH HHS HHSN261200800001ENCI NIH HHS K07 CA140790NCI NIH HHS P30 CA014236NCI NIH HHS R01 CA154823NHLBI NIH HHS HHSN268201100011CNHLBI NIH HHS HHSN268201100011I
6 · The paper itself

Abstract

Because the peroxisome proliferator-activated receptor (PPAR) signaling pathway is involved in development and progression of pancreatic cancer, we investigated associations between genetic variants of the PPAR pathway genes and pancreatic cancer risk by using three published genome-wide association study datasets including 8477 cases and 6946 controls of European ancestry. Expression quantitative trait loci (eQTL) analysis was also performed for correlations between genotypes of the identified genetic variants and messenger RNA (mRNA) expression levels of their genes by using available databases of the 1000 Genomes, TCGA, and GTEx projects. In the single-locus logistic regression analysis, we identified 1141 out of 17 532 significant single-nucleotide polymorphisms (SNPs) in 112 PPAR pathway genes. Further multivariate logistic regression analysis identified three independent, potentially functional loci (rs12947620 in MED1, rs11079651 in PRKCA, and rs34367566 in PRKCB) for pancreatic cancer risk (odds ratio [OR] = 1.11, 95% confidence interval [CI], [1.06-1.17], P = 5.46 × 10

Indexed as

Polymorphism, Single NucleotideAgedBiomarkers, TumorCase-Control StudiesFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenotypeHumansMaleMediator Complex Subunit 1Middle AgedPancreatic NeoplasmsPeroxisome Proliferator-Activated ReceptorsPrognosisBiomarkers, TumorMED1 protein, humanMediator Complex Subunit 1Peroxisome Proliferator-Activated ReceptorsPRKCA protein, humanPRKCB protein, humanProtein Kinase C-alphaProtein Kinase C betagenome-wide association studypancreatic cancer susceptibilitypathway analysisPPARsingle-nucleotide polymorphism

Identifiers

PMID32367578
PMCPMC7592725
OpenAlexW3022951533

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.