Evidence map›Paper›PMID 40932369›Full record

ArticleeLife2025

Dissecting infant leukemia developmental origins with a hemogenic gastruloid model.

Denise Ragusa, Chun Wai Suen, Gabriel Torregrosa Cortes, Fabio Pastorino, Ayona Johns, Ylenia Cicirò, Liza Dijkhuis, Susanne van den Brink, Michele Cilli, Connor Byrne and 9 more

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. N2B27 media formulations influence gastruloid development.Development (Cambridge, England) · 2025
    Article
  6. Review
  7. 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

19 authors.

Denise Ragusa *College of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.ORCID https://orcid.org/0000-0002-0303-8683
Chun Wai Suen *Department of Genetics, University of Cambridge, Cambridge, United Kingdom.
Gabriel Torregrosa Cortes *Department of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain.ORCID https://orcid.org/0000-0003-4528-5663
Fabio Pastorino *Laboratory of Experimental Therapies in Oncology, IRCCS Istituto Giannina Gaslini, Genova, Italy.
Ayona JohnsCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.
Ylenia CiciròCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.ORCID https://orcid.org/0000-0003-1607-3266
Liza DijkhuisCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.
Susanne van den BrinkProgram in Cancer Research, Hospital del Mar Research Institute, CIBERONC, Barcelona, Spain.
Michele CilliAnimal Facility, IRCCS Policlinico San Martino, Genova, Italy.
Connor ByrneCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.
Giulia-Andreea IonescuCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.
Joana CerveiraDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom.
Kamil R KrancCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.
Victor Hernandez-HernandezCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.
Mirco PonzoniLaboratory of Experimental Therapies in Oncology, IRCCS Istituto Giannina Gaslini, Genova, Italy.
Anna BigasProgram in Cancer Research, Hospital del Mar Research Institute, CIBERONC, Barcelona, Spain.ORCID https://orcid.org/0000-0003-4801-6899
Jordi Garcia-OjalvoDepartment of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain.
Alfonso Martínez AriasDepartment of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain.ORCID https://orcid.org/0000-0002-1781-564X
Cristina PinaCollege of Health, Medicine and Life Sciences, Centre for Genome Engineering and Maintenance, Brunel University, London, United Kingdom.ORCID https://orcid.org/0000-0002-2575-6301

Funding

Agencia Estatal de Investigación CEX2018-000792-MAgencia Estatal de Investigación PLEC2021-007518Brunel University London BRIEF Award PinaEuropean Molecular Biology Organization ALTF 195-2021European Research Council MiniEmbryoBlueprint 834580Generalitat de Catalunya ICREA AcademiaHuman Frontier Science Program LT0047/2022-LKay Kendall Leukaemia Fund KL888Lady Tata Memorial Trust Memorial Trust International Scholarship 2022Leuka Leuka John Goldman Fellowship for Future Science 2017-2019Little Princess Trust CCLGA 2023 22 PinaMinisterio de Ciencia e Innovación PGC2018-101251-BI00Ministerio de Universidades FPU18/05091Ministero della Salute Ricerca CorrenteMinistero della Salute Ricerca Finalizzata 5 per milleNational Centre for the Replacement Refinement and Reduction of Animals in Research NC/Z500677/1Royal Society of Biology MRSB Travel Grant RagusaWellcome TrustWellcome Trust ISSF Bridge Funding Award 2019
6 · The paper itself

Abstract

Current in vitro models of developmental blood formation lack spatio-temporal accuracy and weakly replicate successive waves of hematopoiesis. Herein, we describe a mouse embryonic stem cell (SC)-derived 3D hemogenic gastruloid (haemGx) that captures multi-wave blood formation, progenitor specification from hemogenic endothelium (HE), and generates hematopoietic progenitors capable of short-term engraftment of immunodeficient mice upon maturation in an in vivo niche. We took advantage of the haemGx model to interrogate the origins of infant acute myeloid leukemia (infAML). We focused on MNX1-driven leukemia, representing the commonest genetic abnormality unique to the infant group. Enforced MNX1 expression in haemGx promotes the expansion and in vitro transformation of yolk sac-like erythroid-myeloid progenitors at the HE-to-hematopoietic transition to faithfully recapitulate patient transcriptional signatures. By combining phenotypic, functional, and transcriptional profiling, including at the single-cell level, we establish the haemGx as a useful new model for the study of normal and leukemic embryonic hematopoiesis.

Indexed as

HemangioblastsHematopoiesisLeukemia, Myeloid, AcuteMouse Embryonic Stem CellsAnimalsDisease Models, AnimalHematopoietic Stem CellsHumansInfantMiceTranscription FactorsTranscription Factorscancer biologydevelopmentdevelopmental biologygastruloidhematopoiesisleukemiamouse

Identifiers

PMID40932369
PMCPMC12425479

What OpenQuestion holds

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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.