Evidence map›Paper›PMID 42001795›Full record

ArticleNeoplasia (New York, N.Y.)2026

Characterizing the impact of MLL fusion variants and fusion partners on leukemia plasticity using a human CRISPR-engineered MLL-rearranged leukemia model.

Pia Radszuweit, Rahel Fitzel, Sarah Bruestl, Thomas Hentrich, Fulya Korkmaz, Barbara Mankel, Irene González-Menéndez, Saskia Rudat, Rolf Marschalek, Estelle Erkner and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 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. 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.

Pia RadszuweitDepartment of Medical Oncology and Hematology, University Hospital Zurich, Zurich, Switzerland; Department of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Rahel FitzelDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Sarah BruestlDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Thomas HentrichDepartment of Genetics/Epigenetics, Saarland University, Saarbrücken, Germany.
Fulya KorkmazDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Barbara MankelInstitute of Pathology and Neuropathology and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany.
Irene González-MenéndezInstitute of Pathology and Neuropathology and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany; Core Facility Histology, Faculty of Medicine, University of Tübingen, Tübingen, Germany.
Saskia RudatDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Rolf MarschalekInstitute of Pharmaceutical Biology, Goethe-University Frankfurt, Frankfurt/Main, Germany.
Estelle ErknerDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Hildegard KeppelerDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Rebekka SchairerDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Luise LuibDepartment of General Paediatrics, Haematology/Oncology, University Children's Hospital Tübingen, Tübingen, Germany.
Markus MezgerDepartment of General Paediatrics, Haematology/Oncology, University Children's Hospital Tübingen, Tübingen, Germany.
Leticia Quintanilla-MartinezInstitute of Pathology and Neuropathology and Comprehensive Cancer Center, University Hospital Tübingen, Tübingen, Germany; Core Facility Histology, Faculty of Medicine, University of Tübingen, Tübingen, Germany; Cluster of Excellence iFIT (EXC 2180) "Image-Guided and Functionally Instructed Tumor Therapies", Eberhard Karls University, Tübingen, Germany.
Julia Schulze-HentrichDepartment of Genetics/Epigenetics, Saarland University, Saarbrücken, Germany.
Claudia LengerkeDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Dominik SchneidawindDepartment of Medical Oncology and Hematology, University Hospital Zurich, Zurich, Switzerland; Department of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Corina SchneidawindDepartment of Medical Oncology and Hematology, University Hospital Zurich, Zurich, Switzerland; Department of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany. Electronic address: corina.schneidawind@usz.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute leukemias involving KMT2A (MLL) rearrangements are aggressive hematologic malignancies associated with a poor prognosis, especially in infants. The majority of MLL breakpoints are located within the breakpoint cluster region spanning exons 8-14, with AFF1 (AF4) and MLLT3 (AF9) being the most frequent fusion partners. To study the contribution of different fusion partners and breakpoint locations to leukemogenesis, we created a human CRISPR/Cas9-based model. We introduced MLL::AF4 or MLL::AF9 fusions with MLL breakpoints in intron 9 or 11, respectively, into human cord blood-derived CD34

Indexed as

Gene RearrangementHistone-Lysine N-MethyltransferaseLeukemiaMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionAnimalsCRISPR-Cas SystemsDisease Models, AnimalHumansMiceHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionAcute leukemiaCRISPR/Cas9-engineered modelsHematopoetic stem cellsin vivo leukemia modelingKMT2A-rearrangementsLeukemia modeling

Identifiers

PMID42001795
PMCPMC13098342

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.