Evidence map›Paper›PMID 39019934›Full record

ArticleNature communications2024

Selective pressures of platinum compounds shape the evolution of therapy-related myeloid neoplasms.

Eline J M Bertrums, Jurrian K de Kanter, Lucca L M Derks, Mark Verheul, Laurianne Trabut, Markus J van Roosmalen, Henrik Hasle, Evangelia Antoniou, Dirk Reinhardt, Michael N Dworzak and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

15 authors.

Eline J M Bertrums *Princess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.ORCID 0000-0002-0012-7816
Jurrian K de Kanter *Princess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.ORCID 0000-0001-5665-3711
Lucca L M DerksPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.ORCID 0000-0001-9836-5558
Mark VerheulPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.
Laurianne TrabutPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.
Markus J van RoosmalenPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.ORCID 0000-0003-3329-1185
Henrik HasleDepartment of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.ORCID 0000-0003-3976-9231
Evangelia AntoniouClinic of Pediatrics III, University Hospital of Essen, Essen, Germany.
Dirk ReinhardtClinic of Pediatrics III, University Hospital of Essen, Essen, Germany.ORCID 0000-0002-7027-4483
Michael N DworzakSt. Anna Children's Cancer Research Institute, Vienna, Austria.
Nora MühleggerSt. Anna Children's Cancer Research Institute, Vienna, Austria.
Marry M van den Heuvel-EibrinkPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.ORCID 0000-0002-7760-879X
C Michel ZwaanPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.
Bianca F GoemansPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands.ORCID 0000-0003-4030-3228
Ruben van BoxtelPrincess Máxima Centrum for pediatric oncology, Utrecht, the Netherlands. R.vanBoxtel@prinsesmaximacentrum.nl.ORCID 0000-0003-1285-2836

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 864499
6 · The paper itself

Abstract

Therapy-related myeloid neoplasms (t-MN) arise as a complication of chemo- and/or radiotherapy. Although t-MN can occur both in adult and childhood cancer survivors, the mechanisms driving therapy-related leukemogenesis likely vary across different ages. Chemotherapy is thought to induce driver mutations in children, whereas in adults pre-existing mutant clones are selected by the exposure. However, selective pressures induced by chemotherapy early in life are less well studied. Here, we use single-cell whole genome sequencing and phylogenetic inference to show that the founding cell of t-MN in children starts expanding after cessation of platinum exposure. In patients with Li-Fraumeni syndrome, characterized by a germline TP53 mutation, we find that the t-MN already expands during treatment, suggesting that platinum-induced growth inhibition is TP53-dependent. Our results demonstrate that germline aberrations can interact with treatment exposures in inducing t-MN, which is important for the development of more targeted, patient-specific treatment regimens and follow-up.

Indexed as

Germ-Line MutationLi-Fraumeni SyndromeNeoplasms, Second PrimaryTumor Suppressor Protein p53AdolescentAdultAntineoplastic AgentsChildChild, PreschoolFemaleHumansMalePhylogenyPlatinum CompoundsSingle-Cell AnalysisWhole Genome SequencingAntineoplastic AgentsPlatinum CompoundsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID39019934
PMCPMC11255340

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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.