Evidence map›Paper›PMID 26263511›Full record

ArticlePloS one2015

The A Allele at rs13419896 of EPAS1 Is Associated with Enhanced Expression and Poor Prognosis for Non-Small Cell Lung Cancer.

Andika C Putra, Hidetaka Eguchi, Kian Leong Lee, Yuko Yamane, Ewita Gustine, Takeshi Isobe, Masahiko Nishiyama, Keiko Hiyama, Lorenz Poellinger, Keiji Tanimoto

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 19% 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, 45 citations in OpenAlex.

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  10. MiR-519d-3p enhances the sensitivity of non-small-cell lung cancer to tyrosine kinase inhibitors.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
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  14. EPAS1 promotes peritoneal carcinomatosis of non-small-cell lung cancer by enhancing mesothelial-mesenchymal transition.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2021
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  18. Molecular Deregulation ofFrontiers in oncology · 2020
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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

10 authors at 6 institutions in 3 countries.

Andika C PutraDepartment of Radiation Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Hidetaka EguchiDivision of Translational Research, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Kian Leong LeeCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Yuko YamaneDepartment of Radiation Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Ewita GustineDepartment of Radiation Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Takeshi IsobeDivision of Clinical Oncology and Respiratory Medicine, Department of Internal Medicine, School of Medicine, Shimane University, Shimane, Japan.
Masahiko NishiyamaDepartment of Molecular and Cellular Pharmacology, Graduate School of Medicine, Gunma University, Gunma, Japan.
Keiko HiyamaNatural Science Center for Basic Research and Development, Hiroshima University, Hiroshima, Japan.
Lorenz PoellingerCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore; Department of Cell and Molecular Biology, Medical Nobel Institute, Karolinska Institute, Stockholm, Sweden.
Keiji TanimotoDepartment of Radiation Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Hiroshima University · JPGunma University · JPKarolinska Institutet · SENational University Cancer Institute, Singapore · SGSaitama Medical University · JPShimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-inducible factor-2α (HIF-2α, or EPAS1) is important for cancer progression, and is a putative biomarker for poor prognosis for non-small cell lung cancer (NSCLC). However, molecular mechanisms underlying the EPAS1 overexpression are not still fully understood. We explored a role of a single nucleotide polymorphism (SNP), rs13419896 located within intron 1 of the EPAS1 gene in regulation of its expression. Bioinformatic analyses suggested that a region including the rs13419896 SNP plays a role in regulation of the EPAS1 gene expression and the SNP alters the binding activity of transcription factors. In vitro analyses demonstrated that a fragment containing the SNP locus function as a regulatory region and that a fragment with A allele showed higher transactivation activity than one with G, especially in the presence of overexpressed c-Fos or c-Jun. Moreover, NSCLC patients with the A allele showed poorer prognosis than those with G at the SNP even after adjustment with various variables. In conclusion, the genetic polymorphism of the EPAS1 gene may lead to variation of its gene expression levels to drive progression of the cancer and serve as a prognostic marker for NSCLC.

Indexed as

AllelesGene ExpressionPolymorphism, Single NucleotideAgedBasic Helix-Loop-Helix ProteinsCarcinoma, Non-Small-Cell LungCell Line, TumorEndothelial PAS Domain-Containing Protein 1FemaleGene FrequencyGenes, ReporterHumansLung NeoplasmsMaleMiddle AgedNeoplasm StagingBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1

Identifiers

PMID26263511
PMCPMC4532412
OpenAlexW2132037224

What OpenQuestion holds

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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.