Evidence map›Paper›PMID 28152093›Full record

ArticlePloS one2017

Combined effect of genetic polymorphisms of AURKA and environmental factors on oral cancer development in Taiwan.

Chia-Hsuan Chou, Ying-Erh Chou, Chun-Yi Chuang, Shun-Fa Yang, Chiao-Wen Lin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  11. Observational
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  13. Review
  14. The role of Aurora-A in human cancers and future therapeutics.American journal of cancer research · 2020
    Review
  15. Article
  16. Impacts ofJournal of Cancer · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. Lack of associations betweenBioscience reports · 2018
    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

5 authors at 2 institutions in 1 country.

Chia-Hsuan ChouInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Ying-Erh ChouDepartment of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Chun-Yi ChuangSchool of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Chiao-Wen LinInstitute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWChung Shan Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOral squamous cell carcinoma (OSCC) is the sixth and fourth most common cause of cancer death in men worldwide and in Taiwan, respectively. AURKA, which encodes a centrosome-related serine/threonine kinase, is frequently amplified and overexpressed in many human cancers, particularly advanced OSCC. We conducted a hospital-based case-control study to estimate AURKA single-nucleotide polymorphisms (SNPs) and environmental risk factors to determine OSCC susceptibility and clinicopathological characteristics. METHODOLOGY/PRINCIPAL

findingsWe enrolled a total of 876 OSCC patients and 1200 controls. Four SNPs of AURKA, namely rs1047972, rs2273535, rs2064863, and rs6024836, were analyzed using real-time polymerase chain reaction (PCR). Among the 1420 smokers, the AURKA polymorphism carriers with the betel nut chewing habit had a higher risk of oral cancer than AURKA wild-type (WT) carriers without the betel nut chewing habit. Patients with the AURKA rs2064863 gene had a 1.365-fold higher risk of stage III or IV OSCC (95% confidence interval [CI] 1.029-1.811) than those with the rs2064863 WT gene. Furthermore, carriers of the AURKA rs1047972/rs2273535/rs2064863 C-A-T haplotype had a 1.736-fold (95% CI 1.110-2.715) higher risk of OSCC than controls (C-T-T, the most common haplotype). Among patients with the betel quid chewing habit, carriers of other haplotypes (C-T-T, C-A-G, T-A-T, T-A-G, T-T-T, and C-T-G) had a 12.857-fold (95% CI 10.731-15.404) increased risk, and carriers of the C-A-T haplotype had the highest risk (AOR: 31.120; 95% CI 13.864-69.850) of OSCC, compared with those without the betel quid chewing who harbored other haplotypes.

conclusionsIn conclusion, betel nut chewing combined with the AURKA C-A-T haplotypes lead to a high risk of OSCC. These findings reveal a novel genetic-environmental predisposition for oral tumorigenesis.

Indexed as

ArecaAurora Kinase ACarcinoma, Squamous CellCase-Control StudiesGene FrequencyGenetic Predisposition to DiseaseHaplotypesHumansMaleMiddle AgedMouth NeoplasmsPolymorphism, Single NucleotideReal-Time Polymerase Chain ReactionRisk FactorsSmokingTaiwanAURKA protein, humanAurora Kinase A

Identifiers

PMID28152093
PMCPMC5289639
OpenAlexW2584816264

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LicenceCC BY
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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.