Evidence map›Paper›PMID 40694850›Full record

ArticleNucleic acids research2025

Low-amplitude copy number gains shape cancer through known and novel oncogenes with associated therapeutic vulnerabilities.

Thomas F Eleveld, Bauke Ylstra, Leendert H J Looijenga

Abstract read
In one paragraph

Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

3 authors.

Thomas F EleveldPrincess Máxima Center for Pediatric Oncology, Heidelberglaan 25, 3584 CS Utrecht, The Netherlands.ORCID 0000-0001-8580-4822
Bauke YlstraAmsterdam UMC, Vrije Universiteit Amsterdam, Department of Pathology, Cancer Center Amsterdam, 1081 BT Amsterdam, The Netherlands.ORCID 0000-0001-9479-3010
Leendert H J LooijengaPrincess Máxima Center for Pediatric Oncology, Heidelberglaan 25, 3584 CS Utrecht, The Netherlands.

Funding

Dutch Cancer Society KWF 20161-1-10271KIKA
6 · The paper itself

Abstract

Large chromosomal copy number gains are ubiquitous throughout cancer types. However, which genes drive their selective advantage is not well established, and therefore they are hardly utilized in clinical practice. Our analysis of copy number patterns in pan-cancer datasets suggests that the selective advantage of copy number gains is largely driven by known oncogenes. Analysis of CRISPR screening data identifies a list of 101 genes that are likely to mediate the effect of these gains, which is highly enriched in annotated oncogenes but also contains genes that have not been implicated in cancer so far. Moreover, we show that specific gains are associated with drug sensitivity or resistance, with a strong enrichment of gains of oncogenes with increased sensitivity to inhibitors targeting these specific genes. Finally, we provide examples where gains can function as relevant clinical biomarkers for diagnosis and treatment. Thus, large copy number gains exert their selective advantage through known and novel oncogenes, and their systematic analysis could advance precision oncology.

Indexed as

DNA Copy Number VariationsGene DosageNeoplasmsOncogenesBiomarkers, TumorCRISPR-Cas SystemsDrug Resistance, NeoplasmHumansBiomarkers, Tumor

Identifiers

PMID40694850
PMCPMC12282949

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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.