Evidence map›Paper›PMID 29443959›Full record

ArticleNature2018

Transcriptional regulation by NR5A2 links differentiation and inflammation in the pancreas.

Isidoro Cobo, Paola Martinelli, Marta Flández, Latifa Bakiri, Mingfeng Zhang, Enrique Carrillo-de-Santa-Pau, Jinping Jia, Víctor J Sánchez-Arévalo Lobo, Diego Megías, Irene Felipe and 13 more

Open access · greenAbstract read
In one paragraph

Article in Nature, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

91 citing papers in PubMed, 143 citations in OpenAlex.

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31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 9 institutions in 4 countries.

Isidoro CoboEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Paola MartinelliEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Marta FlándezEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Latifa BakiriGenes, Development, and Disease Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Mingfeng ZhangLaboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Enrique Carrillo-de-Santa-PauEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Jinping JiaLaboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Víctor J Sánchez-Arévalo LoboEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Diego MegíasConfocal Microscopy Unit, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Irene FelipeEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Natalia Del PozoEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Irene MillánEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Liv ThommesenDepartment of Biomedical Science, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Torunn BrulandClinic of Medicine, St. Olav's University Hospital, Trondheim, Norway.
Sara H OlsonDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
Jill SmithDepartments of Gastroenterology and Hepatology, Georgetown University, Washington, DC 20007, USA.
Kristina SchoonjansEcole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
William R BamletDivision of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota 55905, USA.
Gloria M PetersenDivision of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota 55905, USA.
Núria MalatsGenetic and Molecular Epidemiology Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Laufey T AmundadottirLaboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Erwin F WagnerGenes, Development, and Disease Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Francisco X RealEpithelial Carcinogenesis Group, Spanish National Cancer Research Centre-CNIO, Madrid, Spain.
Spanish National Cancer Research Centre · ESMayo Clinic in Florida · USNational Institutes of Health · USNorwegian University of Science and Technology · NOCentro de Investigación Biomédica en Red de Cáncer · ESÉcole Polytechnique Fédérale de Lausanne · CHGeorgetown University · USMemorial Sloan Kettering Cancer Center · USNational Cancer Institute · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Laboratory of Translational GenomicsZIACP010201 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI PROKUNINA-OLSSON, LIUDMILA · 2010 to 2025
$91.2M
Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI MUKHOPADHYAY, DEBABRATA · 2004 to 2018
$32.7M
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA102701
6 · The paper itself

Abstract

Chronic inflammation increases the risk of developing one of several types of cancer. Inflammatory responses are currently thought to be controlled by mechanisms that rely on transcriptional networks that are distinct from those involved in cell differentiation. The orphan nuclear receptor NR5A2 participates in a wide variety of processes, including cholesterol and glucose metabolism in the liver, resolution of endoplasmic reticulum stress, intestinal glucocorticoid production, pancreatic development and acinar differentiation. In genome-wide association studies, single nucleotide polymorphisms in the vicinity of NR5A2 have previously been associated with the risk of pancreatic adenocarcinoma. In mice, Nr5a2 heterozygosity sensitizes the pancreas to damage, impairs regeneration and cooperates with mutant Kras in tumour progression. Here, using a global transcriptomic analysis, we describe an epithelial-cell-autonomous basal pre-inflammatory state in the pancreas of Nr5a2

Indexed as

Gene Expression RegulationTranscriptomeAcinar CellsAnimalsCell DifferentiationChromatinEpithelial CellsGene Regulatory NetworksGenes, junHeterozygoteHumansInflammationMiceOrgan SpecificityPancreasPancreatitisChromatinNR5A2 protein, humanNr5a2 protein, mouseReceptors, Cytoplasmic and NuclearTranscription Factor AP-1

Identifiers

PMID29443959
PMCPMC6121728
OpenAlexW2785829537

What OpenQuestion holds

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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.