Evidence map›Paper›PMID 27282650›Full record

ArticleScientific reports2016

Identification of circulating microRNAs during the liver neoplastic process in a murine model of hereditary tyrosinemia type 1.

Francesca Angileri, Geneviève Morrow, Jean-Yves Scoazec, Nicolas Gadot, Vincent Roy, Suli Huang, Tangchun Wu, Robert M Tanguay

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

8 authors at 2 institutions in 2 countries.

Francesca AngileriLaboratoire de génétique cellulaire et développementale, IBIS and PROTEO, Département de biologie moléculaire, biochimie médicale et pathologie, Faculté de médecine, 1030 avenue de la Médecine, Université Laval, Québec, Canada, G1V 0A6.
Geneviève MorrowLaboratoire de génétique cellulaire et développementale, IBIS and PROTEO, Département de biologie moléculaire, biochimie médicale et pathologie, Faculté de médecine, 1030 avenue de la Médecine, Université Laval, Québec, Canada, G1V 0A6.
Jean-Yves ScoazecAnipath, Faculté Laennec, rue Guillaume Paradin, 69372 Lyon Cedex 08, France.
Nicolas GadotAnipath, Faculté Laennec, rue Guillaume Paradin, 69372 Lyon Cedex 08, France.
Vincent RoyLaboratoire de génétique cellulaire et développementale, IBIS and PROTEO, Département de biologie moléculaire, biochimie médicale et pathologie, Faculté de médecine, 1030 avenue de la Médecine, Université Laval, Québec, Canada, G1V 0A6.
Suli HuangDept of Occupational and Environmental Health and Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Tangchun WuDept of Occupational and Environmental Health and Key Laboratory of Environment and Health, Ministry of Education and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Robert M TanguayLaboratoire de génétique cellulaire et développementale, IBIS and PROTEO, Département de biologie moléculaire, biochimie médicale et pathologie, Faculté de médecine, 1030 avenue de la Médecine, Université Laval, Québec, Canada, G1V 0A6.
Université Laval · CAHuazhong University of Science and Technology · CN

Funding

CIHR
6 · The paper itself

Abstract

Hereditary tyrosinemia type 1 (HT1) is a severe inborn error of metabolism, impacting the tyrosine catabolic pathway with a high incidence of hepatocellular carcinoma (HCC). Using a HT1 murine model, we investigated the changes in profiles of circulating and hepatic miRNAs. The aim was to determine if plasma miRNAs could be used as non-invasive markers of liver damage in HT1 progression. Plasma and liver miRNAome was determined by deep sequencing after HT1 phenotype was induced. Sequencing analysis revealed deregulation of several miRNAs including let-7/miR-98 family, miR-21 and miR-148a, during manifestation of liver pathology. Three miRNAs (miR-98, miR-200b, miR-409) presenting the highest plasmatic variations among miRNAs found in both plasma and liver and with >1000 reads in at least one plasma sample, were further validated by RT-qPCR. Two of these miRNAs have protein targets involved in HT1 and significant changes in their circulating levels are detectable prior an increase in protein expression of alpha-fetoprotein, the current biomarker for HCC diagnosis. Future assessment of these miRNAs in HT1 patients and their association with liver neoplastic lesions might designate these molecules as potential biomarkers for monitoring HT1 damage progression, improving diagnosis for early HCC detection and the design of novel therapeutic targets.

Indexed as

alpha-FetoproteinsAnimalsBiomarkers, TumorCarcinoma, HepatocellularCirculating MicroRNADisease Models, AnimalDisease ProgressionGene Expression Regulation, NeoplasticLiverLiver NeoplasmsMaleMiceTyrosinemiasalpha-FetoproteinsBiomarkers, TumorCirculating MicroRNA

Identifiers

PMID27282650
PMCPMC4901289
OpenAlexW2415924001

What OpenQuestion holds

Textmetadata
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.