Evidence map›Paper›PMID 32541781›Full record

ArticleScientific reports2020

Mir34a constrains pancreatic carcinogenesis.

Ana Hidalgo-Sastre, Clara Lubeseder-Martellato, Thomas Engleitner, Katja Steiger, Suyang Zhong, Judit Desztics, Rupert Öllinger, Roland Rad, Roland M Schmid, Heiko Hermeking and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% 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

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

  1. Pooled it
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  10. International journal of biological sciences · 2022
    Article
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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

12 authors at 4 institutions in 1 country.

Ana Hidalgo-SastreKlinik und Poliklinik für Innere Medizin II, Technical University of Munich, Munich, Germany.
Clara Lubeseder-MartellatoKlinik und Poliklinik für Innere Medizin II, Technical University of Munich, Munich, Germany.
Thomas EngleitnerInstitute of Molecular Oncology and Functional Genomics, Department of Medicine II and TranslaTUM Cancer Center, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Katja SteigerInstitute of Pathology, Technical University of Munich, Munich, Germany.
Suyang ZhongKlinik und Poliklinik für Innere Medizin II, Technical University of Munich, Munich, Germany.
Judit DeszticsKlinik und Poliklinik für Innere Medizin II, Technical University of Munich, Munich, Germany.
Rupert ÖllingerInstitute of Molecular Oncology and Functional Genomics, Department of Medicine II and TranslaTUM Cancer Center, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Roland RadInstitute of Molecular Oncology and Functional Genomics, Department of Medicine II and TranslaTUM Cancer Center, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Roland M SchmidKlinik und Poliklinik für Innere Medizin II, Technical University of Munich, Munich, Germany.
Heiko HermekingExperimental and Molecular Pathology, Institute of Pathology, Ludwig Maximilian University Munich, Munich, Germany.
Jens T SivekeInstitute for Developmental Cancer Therapeutics, West German Cancer Center, University Hospital Essen, Essen, Germany.
Guido von FiguraKlinik und Poliklinik für Innere Medizin II, Technical University of Munich, Munich, Germany. gvfigura@tum.de.
Technical University of Munich · DEKlinikum rechts der Isar · DEDeutschen Konsortium für Translationale Krebsforschung · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have shown that over 70 different microRNAs are aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC), affecting proliferation, apoptosis, metabolism, EMT and metastasis. The most important genetic alterations driving PDAC are a constitutive active mutation of the oncogene Kras and loss of function of the tumour suppressor Tp53 gene. Since the MicroRNA 34a (Mir34a) is a direct target of Tp53 it may critically contribute to the suppression of PDAC. Mir34a is epigenetically silenced in numerous cancers, including PDAC, where Mir34a down-regulation has been associated with poor patient prognosis. To determine whether Mir34a represents a suppressor of PDAC formation we generated an in vivo PDAC-mouse model harbouring pancreas-specific loss of Mir34a (Kras

Indexed as

Down-RegulationAnimalsCarcinoma, Pancreatic DuctalGene Expression Regulation, NeoplasticHigh-Throughput Nucleotide SequencingInterleukin-6MiceMicroRNAsPancreatic NeoplasmsPhenotypeProto-Oncogene Proteins p21(ras)Sequence Analysis, RNATumor Necrosis Factor-alphaHras protein, mouseInterleukin-6interleukin-6, mouseMicroRNAsMIRN34a microRNA, mouseProto-Oncogene Proteins p21(ras)Tnf protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID32541781
PMCPMC7295749
OpenAlexW3034189206

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.