Evidence map›Paper›PMID 39760438›Full record

ArticleAdvanced biology2025

Depletion of TP53 in Human Pluripotent Stem Cells Triggers Malignant-Like Behavior.

Joaquin Montilla-Rojo, Thomas F Eleveld, Marnix van Soest, Sanne Hillenius, Dennis M Timmerman, Ad J M Gillis, Bernard A J Roelen, Christine L Mummery, Leendert H J Looijenga, Daniela C F Salvatori

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Article in Advanced biology, 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. Review
  2. 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

10 authors.

Joaquin Montilla-RojoAnatomy and Physiology, Department Clinical Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, 3584 CL, The Netherlands.ORCID https://orcid.org/0000-0002-3168-0796
Thomas F EleveldPrincess Máxima Center for Pediatric Oncology, Utrecht, 3584 CS, The Netherlands.
Marnix van SoestAnatomy and Physiology, Department Clinical Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, 3584 CL, The Netherlands.
Sanne HilleniusPrincess Máxima Center for Pediatric Oncology, Utrecht, 3584 CS, The Netherlands.
Dennis M TimmermanPrincess Máxima Center for Pediatric Oncology, Utrecht, 3584 CS, The Netherlands.
Ad J M GillisPrincess Máxima Center for Pediatric Oncology, Utrecht, 3584 CS, The Netherlands.
Bernard A J RoelenAnatomy and Physiology, Department Clinical Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, 3584 CL, The Netherlands.
Christine L MummeryDepartment of Anatomy and Embryology, Leiden University Medical Centre, Leiden, 2333 ZC, The Netherlands.
Leendert H J LooijengaPrincess Máxima Center for Pediatric Oncology, Utrecht, 3584 CS, The Netherlands.
Daniela C F SalvatoriAnatomy and Physiology, Department Clinical Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, 3584 CL, The Netherlands.ORCID https://orcid.org/0009-0005-3006-8502

Funding

Novo Nordisk Foundation Center for Stem Cell Medicine reNEW NNF21CC0073729Stichting Kinderen Kankervrij 184.034.019
6 · The paper itself

Abstract

Human pluripotent stem cells (hPSCs) tend to acquire genetic aberrations upon culture in vitro. Common aberrations are mutations in the tumor suppressor TP53, suspected to confer a growth-advantage to the mutant cells. However, their full impact in the development of malignant features and safety of hPSCs for downstream applications is yet to be elucidated. Here, TP53 is knocked out in hPSCs using CRISPR-Cas9 and compared them with isogenic wild-type hPSCs and human germ cell tumor lines as models of malignancy. While no major changes in proliferation, pluripotency, and transcriptomic profiles are found, mutant lines display aberrations in some of the main chromosomal hotspots for genetic abnormalities in hPSCs. Additionally, enhanced clonogenic and anchorage-free growth, alongside resistance to chemotherapeutic compounds is observed. The results indicate that common TP53-depleting mutations in hPSCs, although potentially overlooked by standard analyses, can impact their behavior and safety in a clinical setting.

Indexed as

Pluripotent Stem CellsTumor Suppressor Protein p53Cell ProliferationCRISPR-Cas SystemsHumansMutationTP53 protein, humanTumor Suppressor Protein p53genetic aberrationhuman germ cell tumorhuman pluripotent stem cellmalignancypluripotencyTP53

Identifiers

PMID39760438
PMCPMC12001006

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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.