Evidence map›Paper›PMID 41130277›Full record

ArticleEuropean journal of haematology2026

Clonal Progression and Leukemic Transformation of a TP53 Mutated Post-Polycythaemia Vera Myelofibrosis.

Isidor Minović, Bart Koopman, Joris J W Ploegmakers, Elise M J van der Logt, Arjen H G Cleven, Anouk van der Veen, Arjan Buijs, André B Mulder, Emanuele Ammatuna

Abstract readCase Reports
In one paragraph

Article in European journal of haematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Isidor MinovićDepartment of Laboratory Medicine, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0002-5439-3781
Bart KoopmanDepartment of Pathology and Medical Biology, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.ORCID https://orcid.org/0000-0003-0873-9638
Joris J W PloegmakersDepartment of Orthopaedic Surgery, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
Elise M J van der LogtDepartment of Pathology and Medical Biology, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
Arjen H G ClevenDepartment of Pathology and Medical Biology, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
Anouk van der VeenDepartment of Genetics, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
Arjan BuijsDepartment of Genetics, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
André B MulderDepartment of Laboratory Medicine, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.
Emanuele AmmatunaDepartment of Haematology, University of Groningen, University Medical Centre Groningen, Groningen, the Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies investigating the role of TP53 mutations in chronic phase MPN have yielded inconsistent results. As such, the clinical relevance of these mutations remains to be elucidated. We report a case of a 67-year-old woman with a leukemic transformation of a post-polycythaemia vera myelofibrosis (post-PV MF) that culminated in the rare development of a myeloid sarcoma. During a 4-year follow-up, the patient had a stable JAK2 Val617Phe and NFE2 mutation (Variant Allele Frequencies (VAF's) 85%-87% and 43%-50%, respectively) and low-burden TP53 mutation (VAF 2%-7%) in blood and bone marrow. Despite having a low-risk post-PV MF, the patient soon presented with an aggressive lytic lesion in the humerus, which proved to be a myeloid sarcoma. The sarcoma was positive for JAK2 Val617Phe but, interestingly, was also highly enriched for the TP53 mutation (VAF 81%), implicating a role of the TP53 mutation in the leukemic progression. This case provides molecular evidence that a TP53 mutation, even at a low burden, may contribute to leukemic progression of a chronic phase myeloproliferative neoplasm (MPN). These observations increase our understanding of the pathophysiologic behavior of TP53 mutations and underscore the importance of further causal research towards the clinical implications of these mutations in chronic phase MPN.

Indexed as

Cell Transformation, NeoplasticClonal EvolutionMutationPolycythemia VeraPrimary MyelofibrosisTumor Suppressor Protein p53AgedDisease ProgressionFemaleHumansJanus Kinase 2JAK2 protein, humanJanus Kinase 2TP53 protein, humanTumor Suppressor Protein p53chloromaleukemiamyelofibrosismyeloid sarcomapolycythaemia vera

Identifiers

PMID41130277
PMCPMC12673350

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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.