Evidence map›Paper›PMID 41123840›Full record

ReviewCurrent oncology reports2025

Genetically Modified Mouse Models for Sarcoma Research: A Comprehensive Review.

Piotr Remiszewski, Eryk Siedlecki, Marlena Wełniak-Kamińska, Michał Mikula, Anna M Czarnecka

Abstract readReview
In one paragraph

Review in Current oncology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Choosing the right animal model for sarcoma research.Cellular and molecular life sciences : CMLS · 2026
    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

5 authors.

Piotr RemiszewskiDepartment of Soft Tissue/Bone Sarcoma and Melanoma, Maria Sklodowska- Curie National Research Institute of Oncology, Warsaw, Poland.
Eryk SiedleckiDepartment of Soft Tissue/Bone Sarcoma and Melanoma, Maria Sklodowska- Curie National Research Institute of Oncology, Warsaw, Poland.
Marlena Wełniak-KamińskaSmall Animal Magnetic Resonance Imaging Laboratory, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland.
Michał MikulaDepartment of Genetics, Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, 02-781, Poland.
Anna M CzarneckaDepartment of Soft Tissue/Bone Sarcoma and Melanoma, Maria Sklodowska- Curie National Research Institute of Oncology, Warsaw, Poland. anna.czarnecka@gmail.com.

Funding

Narodowe Centrum Nauki 2019/35/O/NZ2/03761 (AMC)
6 · The paper itself

Abstract

purpose of reviewSarcomas are a heterogeneous group of over 170 malignant tumours of mesenchymal origin. The poor prognosis highlights the need for novel therapeutic strategies. Preclinical modelling is essential, yet challenging, given that sarcomas differ substantially from carcinomas and resources are very limited. RECENT

findingsGEMMs allow for the precise modelling of recurrent sarcoma genetics. The Cre-loxP system offer spatial and temporal control over the activation of oncogenes or the loss of tumour suppressors, while the CRISPR-Cas9 system enables the rapid, simultaneous editing of key drivers such as Trp53, Nf1, Kras and Pten. These models reproduce key features of human sarcomas, including their histopathology, the initiation of tumours in specific lineages and sites, and tumour-immune interactions within immune-competent hosts. GEMMs have been used to investigate hypotheses about the cells of origin, to test radiotherapy and immunotherapy, and to compare fusion-driven sarcomas with those with a complex karyotype. Despite variability, GEMMs remain essential tools for investigating the mechanisms of initiation, progression, and response to therapy. GEMMs offer mechanistic fidelity, but their use is limited by factors such as breeding burden, variability in recombination, off-target effects of CRISPR, underrepresentation of genomic complexity and inconsistent metastasis. These weaknesses reduce their predictive value, particularly with regard to advanced disease and immunotherapy. Progress will require the integration of Cre-loxP with CRISPR-Cas9, the standardisation of induction and reporting, and a closer alignment with distinct sarcoma subtypes, in order to enhance translational relevance.

Indexed as

Disease Models, AnimalSarcomaAnimalsAnimals, Genetically ModifiedCRISPR-Cas SystemsGene EditingHumansMiceAnimal modelsCre-loxPCRISPR-Cas9Genetically engineered mousePreclinical modelSoft tissue sarcoma

Identifiers

PMID41123840
PMCPMC12698823

What OpenQuestion holds

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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.