Evidence map›Paper›PMID 41035915›Full record

ArticleFrontiers in pharmacology2025

The role of the lysine histone methylase KMT2D in chronic myeloid leukemia.

Lina Schlemminger, Inga Nagel, Inga Vater, Ingolf Cascorbi, Meike Kaehler

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PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 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. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 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.

Lina SchlemmingerInstitute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Inga NagelInstitute of Human Genetics, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Inga VaterInstitute of Human Genetics, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Ingolf CascorbiInstitute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.
Meike KaehlerInstitute of Experimental and Clinical Pharmacology, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) can be effectively treated inhibiting the disease-causing BCR::ABL1 kinase by tyrosine kinase inhibitors (TKIs). Although therapy is initially tremendously successful, resistance may occur in up to 25% of CML patients. Besides aberrations in the BCR::ABL1 kinase domain, a variety of resistance mechanisms are currently discussed, among them epigenetic reprogramming. The histone-modifying enzyme lysine methyltransferase 2D (KMT2D/MLL2) belongs to the most frequently mutated genes in cancer and is also known for its association with hereditary Kabuki syndrome. However, its role in CML is widely unknown. In the present study, we analyzed the role of the

Indexed as

chronic myeloid leukemiadrug resistanceepigeneticshistone modificationimatinibKMT2D

Identifiers

PMID41035915
PMCPMC12481891

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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.