Evidence map›Paper›PMID 42259789›Full record

ArticleNature communications2026

Single-cell whole-genome sequencing reveals convergent evolution in Burkitt lymphoma.

Alexander S Steemers, Markus J van Roosmalen, Rico Hagelaar, Laurianne Trabut, Mark Verheul, Jurrian K de Kanter, Siem Jongsma, Lucca L M Derks, Alexander R Blackwell, Friederike Meyer-Wentrup and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Alexander S SteemersPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0002-7162-7279
Markus J van RoosmalenPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0003-3329-1185
Rico HagelaarPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0003-1622-6293
Laurianne TrabutPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Mark VerheulPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0002-2416-7492
Jurrian K de KanterPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0001-5665-3711
Siem JongsmaPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Lucca L M DerksPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0001-9836-5558
Alexander R BlackwellPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.ORCID http://orcid.org/0000-0002-0369-4584
Friederike Meyer-WentrupPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.
Ruben van BoxtelPrincess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands. R.vanBoxtel@prinsesmaximacentrum.nl.ORCID http://orcid.org/0000-0003-1285-2836

Funding

Stichting Kinderen Kankervrij (KiKa) 424
6 · The paper itself

Abstract

Burkitt lymphoma carries multiple oncogenic drivers yet arises predominantly in children, whose normal cells harbour few age-related mutations. To investigate this paradox, we seek to define the sequence and timing of mutational drivers underlying Burkitt lymphoma development. Here, we analyse single-cell whole-genome sequencing data of 250 paired normal and malignant B-cells from Burkitt lymphoma patients and integrate this data with 21 bulk WGS samples and an existing dataset of 157 clonally expanded B-cells from healthy individuals. Phylogenetic reconstruction reveals an accelerated accumulation of mutations following the emergence of the most recent common ancestor, leading to the early establishment of extensive genetic intratumoural heterogeneity. We further provide evidence that convergent evolution shapes this diversity at both the point mutation- and copy number variation-levels. This in-depth characterisation further establishes Burkitt lymphoma as a paradigmatic model of tumorigenesis with implications for therapeutic intervention.

Indexed as

Burkitt LymphomaEvolution, MolecularWhole Genome SequencingB-LymphocytesDNA Copy Number VariationsHumansMutationPhylogenyPoint MutationSingle-Cell Analysis

Identifiers

PMID42259789
PMCPMC13402838

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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.