Evidence map›Paper›PMID 36230794›Full record

ArticleCancers2022

Molecular Characterization Reveals Subclasses of 1q Gain in Intermediate Risk Wilms Tumors.

Ianthe A E M van Belzen, Marc van Tuil, Shashi Badloe, Eric Strengman, Alex Janse, Eugène T P Verwiel, Douwe F M van der Leest, Sam de Vos, John Baker-Hernandez, Alissa Groenendijk and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. 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 at 3 institutions in 1 country.

Ianthe A E M van BelzenPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Marc van TuilPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Shashi BadloePrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Eric StrengmanPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0001-9796-0507
Alex JansePrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0002-7766-787X
Eugène T P VerwielPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0001-9663-6780
Douwe F M van der LeestPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Sam de VosPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
John Baker-HernandezPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Alissa GroenendijkPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Ronald de KrijgerPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Hindrik H D KerstensPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Jarno DrostPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0002-2941-6179
Marry M van den Heuvel-EibrinkPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Bastiaan B J TopsPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Frank C P HolstegePrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Patrick KemmerenPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.ORCID 0000-0003-2237-7354
Jayne Y Hehir-KwaPrincess Máxima Center for Pediatric Oncology, 3584 CS Utrecht, The Netherlands.
Princess Máxima Center · NLOncode Institute · NLUtrecht University · NL

Funding

Adessium Foundation NAFoundation KiKa NA
6 · The paper itself

Abstract

Chromosomal alterations have recurrently been identified in Wilms tumors (WTs) and some are associated with poor prognosis. Gain of 1q (1q+) is of special interest given its high prevalence and is currently actively studied for its prognostic value. However, the underlying mutational mechanisms and functional effects remain unknown. In a national unbiased cohort of 30 primary WTs, we integrated somatic SNVs, CNs and SVs with expression data and distinguished four clusters characterized by affected biological processes: muscle differentiation, immune system, kidney development and proliferation. Combined genome-wide CN and SV profiles showed that tumors profoundly differ in both their types of 1q+ and genomic stability and can be grouped into WTs with co-occurring 1p-/1q+, multiple chromosomal gains or CN neutral tumors. We identified 1q+ in eight tumors that differ in mutational mechanisms, subsequent rearrangements and genomic contexts. Moreover, 1q+ tumors were present in all four expression clusters reflecting activation of various biological processes, and individual tumors overexpress different genes on 1q. In conclusion, by integrating CNs, SVs and gene expression, we identified subgroups of 1q+ tumors reflecting differences in the functional effect of 1q gain, indicating that expression data is likely needed for further risk stratification of 1q+ WTs.

Indexed as

1q gaincancer genomicschromosomal alterationspediatric cancerRNA-seqstructural variationWGSWilms tumor

Identifiers

PMID36230794
PMCPMC9564324
OpenAlexW4303622001

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.