Evidence map›Paper›PMID 25763109›Full record

ArticleGenome medicine2015

Comparative methylome analysis identifies new tumour subtypes and biomarkers for transformation of nephrogenic rests into Wilms tumour.

Jocelyn Charlton, Richard D Williams, Neil J Sebire, Sergey Popov, Gordan Vujanic, Tasnim Chagtai, Marisa Alcaide-German, Tiffany Morris, Lee M Butcher, Paul Guilhamon and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genome medicine, 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
2.7field-weighted citation impact, top 9% 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.

  1. Trial
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  11. Review
  12. Article
  13. Article
  14. Embryonal precursors of Wilms tumor.Science (New York, N.Y.) · 2019
    Article
  15. Annals of translational medicine · 2019
    Article
  16. Article
  17. The genetic changes of Wilms tumour.Nature reviews. Nephrology · 2019
    Review
  18. Bioscience reports · 2019
    Article
  19. Article
  20. Reply to Brioude et al.European journal of human genetics : EJHG · 2018
    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

12 authors at 2 institutions in 1 country.

Jocelyn CharltonUCL Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH UK.
Richard D WilliamsUCL Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH UK.
Neil J SebireUCL Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH UK.
Sergey PopovThe Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG UK.
Gordan VujanicDepartment of Pathology, Cardiff University School of Medicine, Heath Park, Cardiff, CF14 4XN UK.
Tasnim ChagtaiUCL Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH UK.
Marisa Alcaide-GermanUCL Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH UK.
Tiffany MorrisUCL Cancer Institute, University College London, 72 Huntley Street, London, WC1E 6BT UK.
Lee M ButcherUCL Cancer Institute, University College London, 72 Huntley Street, London, WC1E 6BT UK.
Paul GuilhamonUCL Cancer Institute, University College London, 72 Huntley Street, London, WC1E 6BT UK.
Stephan BeckUCL Cancer Institute, University College London, 72 Huntley Street, London, WC1E 6BT UK.
Kathy Pritchard-JonesUCL Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH UK.
University College London · GBInstitute of Cancer Research · GB

Funding

Cancer Research UK 17297
6 · The paper itself

Abstract

backgroundWilms tumours (WTs) are characterised by several hallmarks that suggest epimutations such as aberrant DNA methylation are involved in tumour progression: loss of imprinting at 11p15, lack of recurrent mutations and formation of nephrogenic rests (NRs), which are lesions of retained undifferentiated embryonic tissue that can give rise to WTs.

methodsTo identify such epimutations, we performed a comprehensive methylome analysis on 20 matched trios of micro-dissected WTs, NRs and surrounding normal kidneys (NKs) using Illumina Infinium HumanMethylation450 Bead Chips and functionally validated findings using RNA sequencing.

resultsComparison of NRs with NK revealed prominent tissue biomarkers: 629 differentially methylated regions, of which 55% were hypermethylated and enriched for domains that are bivalent in embryonic stem cells and for genes expressed during development (P = 2.49 × 10(-5)). Comparison of WTs with NRs revealed two WT subgroups; group-2 WTs and NRs were epigenetically indistinguishable whereas group-1 WTs showed an increase in methylation variability, hypomethylation of renal development genes, hypermethylation and relative loss of expression of cell adhesion genes and known and potential new WT tumour suppressor genes (CASP8, H19, MIR195, RB1 and TSPAN32) and was strongly associated with bilateral disease (P = 0.032). Comparison of WTs and NRs to embryonic kidney highlighted the significance of polycomb target methylation in Wilms tumourigenesis.

conclusionsMethylation levels vary during cancer evolution. We have described biomarkers related to WT evolution from its precursor NRs which may be useful to differentiate between these tissues for patients with bilateral disease.

Identifiers

PMID25763109
PMCPMC4354990
OpenAlexW2108419656

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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.