Evidence map›Paper›PMID 33012783›Full record

ArticleBritish journal of cancer2021

Clinically and biologically relevant subgroups of Wilms tumour defined by genomic and epigenomic analyses.

Jack Brzezinski, Sanaa Choufani, Rodrigo Romao, Cheryl Shuman, Haiying Chen, Joanna Cunanan, Darius Bagli, Ronald Grant, Armando Lorenzo, Rosanna Weksberg

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

Jack BrzezinskiInstitute of Medical Sciences, University of Toronto, Toronto, ON, Canada.
Sanaa ChoufaniGenetics and Genome Biology Program, Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Rodrigo RomaoDepartment of Surgery, IWK Hospital, Halifax, NS, Canada.
Cheryl ShumanDepartment of Pediatrics, Division of Clinical Genetics, Hospital for Sick Children, Toronto, ON, Canada.
Haiying ChenDepartment of Pediatric Laboratory Medicine, Hospital for Sick Children, Toronto, ON, Canada.
Joanna CunananMedical Sciences Graduate Program, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada.
Darius BagliInstitute of Medical Sciences, University of Toronto, Toronto, ON, Canada.
Ronald GrantDepartment of Pediatrics, Division of Hematology and Oncology, Hospital for Sick Children, Toronto, ON, Canada.
Armando LorenzoDepartment of Surgery, Division of Urology, Hospital for Sick Children, Toronto, ON, Canada.
Rosanna WeksbergInstitute of Medical Sciences, University of Toronto, Toronto, ON, Canada. rweksb@sickkids.ca.ORCID http://orcid.org/0000-0002-6501-4150
Hospital for Sick Children · CAUniversity of Toronto · CAIzaak Walton Killam Health Centre · CAMcMaster University · CA

Funding

NCTN BIQSFP ANBL1531 (NRT)U10CA180886 · NCI · PUBLIC HEALTH INSTITUTE · PI Douglas S. Hawkins · 2014 to 2026
$390.6M
COG U24 Funding 2026-2027U24CA196173 · NCI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI Mignon Lee-Cheun Loh, Nilsa Del Carmen Ramirez Milan · 2015 to 2026
$62.5M
NCI NIH HHS U10 CA180886NCI NIH HHS U24 CA196173
6 · The paper itself

Abstract

backgroundAlthough cure rates for Wilms tumours (WT) are high, many patients receive therapy with attendant long-term complications. Our goal was to stratify WT using genome-wide analyses to identify candidate molecular features for patients who would benefit from a reduction in therapy.

methodsWe generated DNA methylation and exome sequencing data on WT-kidney pairs (n = 57) and unpaired tumours (n = 27) collected either at our centre or by the Children's Oncology Group. Samples were divided into a discovery set (n = 32) and validation set (n = 52).

resultsAnalysis of DNA methylation revealed two subgroups of WT with distinct features. Subgroup A has a similar DNA methylation profile to mature kidney, while Subgroup B has genome-wide dysregulation of DNA methylation. The rate of non-synonymous missense mutations and segmental chromosomal aberrations was higher in Subgroup B tumours, suggesting that this group has genome instability related to its epigenetic state. Subgroup A had a higher proportion of cases of bilateral disease. Tumours with high-risk histology or from patients who relapsed were only found in Subgroup B.

conclusionWe have identified subgroup-specific molecular events that could inform future work supporting more targeted therapeutic approaches and patient stratification. We propose a novel developmental tumour model based on these findings.

Indexed as

ChildChromosome AberrationsDNA MethylationExome SequencingFemaleGene Expression ProfilingGenes, Wilms TumorHumansKidney NeoplasmsMaleMutationWilms Tumor

Identifiers

PMID33012783
PMCPMC7853092
OpenAlexW3090245160

What OpenQuestion holds

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LicenceCC BY
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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.