Evidence map›Paper›PMID 30794721›Full record

ArticleCarcinogenesis2019

Potential functional variants in SMC2 and TP53 in the AURORA pathway genes and risk of pancreatic cancer.

Yun Feng, Hongliang Liu, Bensong Duan, Zhensheng Liu, James Abbruzzese, Kyle M Walsh, Xuefeng Zhang, Qingyi Wei

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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  16. Associations of novel variants inAmerican journal of cancer research · 2020
    Article
  17. Is there a CDKN2A-centric networkOncoTargets and therapy · 2020
    Review
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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

8 authors at 2 institutions in 2 countries.

Yun FengDepartment of Respiration, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Hongliang LiuDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
Bensong DuanDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
Zhensheng LiuDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
James AbbruzzeseDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
Kyle M WalshDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
Xuefeng ZhangDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
Qingyi WeiDuke Cancer Institute, Duke University Medical Center, Durham, NC, USA.
Duke University · USTongji University · CN

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI JOHN N. NORTON · 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
Howard 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

The AURORA pathway participates in mitosis and cell division, and alterations in mitosis and cell division can lead to carcinogenesis. Therefore, genetic variants in the AURORA pathway genes may be associated with susceptibility to pancreatic cancer. To test this hypothesis, we used three large publically available pancreatic cancer genome-wide association study (GWAS) datasets (PanScan I, II/III and PanC4) to assess the associations of 7168 single nucleotide polymorphisms (SNPs) in a set of 62 genes of this pathway with pancreatic cancer risk in 8477 cases and 6946 controls of European ancestry. We identify 15 significant pancreatic cancer risk-associated SNPs in three genes (SMC2, ARHGEF7 and TP53) after correction for multiple comparisons by a false discovery rate < 0.20. Through further linkage disequilibrium analysis, SNP functional prediction and stepwise logistic regression analysis, we focused on three SNPs: rs3818626 in SMC2, rs79447092 in ARHGEF7 and rs9895829 in TP53. We found that these three SNPs were associated with pancreatic cancer risk [odds ratio (OR) = 1.12, 95% confidence interval (CI) = 1.07-1.17 and P = 2.20E-06 for the rs3818626 C allele; OR = 0.76, CI = 0.66-0.88 and P = 1.46E-04 for the rs79447092 A allele and OR = 0.82, CI = 0.74-0.91 and P = 1.51E-04 for the rs9895829 G allele]. Their joint effect as the number of protective genotypes also showed a significant association with pancreatic cancer risk (trend test P ≤ 0.001). Finally, we performed an expression quantitative trait loci analysis and found that rs3818626 and rs9895829 were significantly associated with SMC2 and TP53 messenger RNA expression levels in 373 lymphoblastoid cell lines, respectively. In conclusion, these three representative SNPs may be potentially susceptibility loci for pancreatic cancer and warrant additional validation.

Indexed as

AgedAllelesAurora KinasesCase-Control StudiesCell Cycle ProteinsFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansLinkage DisequilibriumMaleMiddle AgedPancreasPancreatic NeoplasmsPolymorphism, Single NucleotideAurora KinasesCell Cycle ProteinsSMC2 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID30794721
PMCPMC6556704
OpenAlexW2916259439

What OpenQuestion holds

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Registered trials

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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.