Evidence map›Paper›PMID 26035382›Full record

ArticleDisease models & mechanisms2015

Deducing the stage of origin of Wilms' tumours from a developmental series of Wt1-mutant mice.

Rachel L Berry, Derya D Ozdemir, Bruce Aronow, Nils O Lindström, Tatiana Dudnakova, Anna Thornburn, Paul Perry, Richard Baldock, Chris Armit, Anagha Joshi and 8 more

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Characterization of Alternative Splicing in High-Risk Wilms' Tumors.International journal of molecular sciences · 2024
    Article
  4. Review
  5. Article
  6. Principles of human and mouse nephron development.Nature reviews. Nephrology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Editorial: WT1 in Development and Disease.Frontiers in cell and developmental biology · 2022
    Article
  11. Article
  12. Review
  13. Frontiers in cell and developmental biology · 2021
    Review
  14. Article
  15. Article
  16. 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

18 authors.

Rachel L BerryMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Derya D OzdemirMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK The Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, UK.
Bruce AronowDepartment of Biomedical Informatics and Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Nils O LindströmMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK The Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, UK.
Tatiana DudnakovaMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Anna ThornburnMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Paul PerryMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Richard BaldockMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Chris ArmitMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Anagha JoshiThe Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, UK.
Cécile JeanpierreINSERM, UMR 1163, Laboratory of Inherited Kidney Diseases, Paris 75015, France Paris Descartes - Sorbonne Paris Cité University, Imagine Institute, Paris 75015, France.
Jingdong ShanBiocenter Oulu, InfoTech Oulu, Faculty of Biochemistry and Molecular Medicine, Aapistie 5A, University of Oulu, PO Box 5000, Oulu 90014, Finland.
Seppo VainioBiocenter Oulu, InfoTech Oulu, Faculty of Biochemistry and Molecular Medicine, Aapistie 5A, University of Oulu, PO Box 5000, Oulu 90014, Finland.
James BailyQueen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.
David BrownsteinQueen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.
Jamie DaviesCentre for Integrative Physiology, University of Edinburgh, Hugh Robson Building, 15 George Square, Edinburgh, EH8 9XD, UK.
Nicholas D HastieMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK.
Peter HohensteinMRC Human Genetics Unit, MRC Institute for Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK The Roslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, UK peter.hohenstein@roslin.ed.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/J004316/1Medical Research Council MC_PC_U127527180Medical Research Council MC_PC_U127527203Medical Research Council MR/K010735/1Medical Research Council MR/M010341/1National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K500549/1Wellcome Trust
6 · The paper itself

Abstract

Wilms' tumours, paediatric kidney cancers, are the archetypal example of tumours caused through the disruption of normal development. The genetically best-defined subgroup of Wilms' tumours is the group caused by biallelic loss of the WT1 tumour suppressor gene. Here, we describe a developmental series of mouse models with conditional loss of Wt1 in different stages of nephron development before and after the mesenchymal-to-epithelial transition (MET). We demonstrate that Wt1 is essential for normal development at all kidney developmental stages under study. Comparison of genome-wide expression data from the mutant mouse models with human tumour material of mutant or wild-type WT1 datasets identified the stage of origin of human WT1-mutant tumours, and emphasizes fundamental differences between the two human tumour groups due to different developmental stages of origin.

Indexed as

AnimalsBiomarkersCell LineageGene Expression Regulation, NeoplasticGenomeIntegrasesMice, Inbred C57BLMice, Mutant StrainsNeoplasm StagingNephronsOligonucleotide Array Sequence AnalysisPhenotypeTime-Lapse ImagingWilms TumorWT1 ProteinsBiomarkersCre recombinaseIntegrasesWT1 ProteinsKidney developmentMouse modelWilms’ tumourWT1

Identifiers

PMID26035382
PMCPMC4527280

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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.