Evidence map›Paper›PMID 41441935›Full record

ReviewMedical oncology (Northwood, London, England)2025

KMT2A-Mediated transcriptional regulation in stemness and cancer: molecular mechanisms and therapeutic opportunities.

Md Shiblee Sadik Sabuj, Tanvir Ahmed, Md Jamilur Rahman, S M Abdus Salam, Byung-Yong Park, Md Rashedunnabi Akanda

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 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. 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

6 authors.

Md Shiblee Sadik SabujCollege of Veterinary Medicine, Institute of Animal Transplantation, Jeonbuk National University, Iksan, 54596, South Korea.
Tanvir AhmedFaculty of Veterinary Medicine, Jashore University of Science and Technology, Jashore, 7408, Bangladesh.
Md Jamilur RahmanCollege of Veterinary Medicine, Kangwon National University, Chuncheon, 24341, South Korea.
S M Abdus SalamChonnam National University Medical School and Hwasun Hospital, Hwasun, 58128, South Korea.
Byung-Yong ParkCollege of Veterinary Medicine, Institute of Animal Transplantation, Jeonbuk National University, Iksan, 54596, South Korea.
Md Rashedunnabi AkandaDepartment of Pharmacology and Toxicology, Sylhet Agricultural University, Sylhet, 3100, Bangladesh. akandamr.dph@sau.ac.bd.ORCID http://orcid.org/0000-0002-5464-9353

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KMT2A (MLL1) is an epigenetic enzyme that activates genes via the addition of histone H3 at lysine 4 (H3K4). As a principal component of the COMPASS (complex of proteins associated with Set1), KMT2A coordinates the transcription of key developmental and lineage-specific genes, thereby shaping cellular plasticity, differentiation, and self-renewal. It is critical for regulating the balance between stem cell renewal and differentiation in both physiological and pathological aspects. Abnormal regulation or chromosomal translocations involving KMT2A are frequently implicated in hematologic malignancies and developmental disorders. In leukemias and other cancers, KMT2A fusion proteins disrupt regular transcriptional programs, creating a tumor-permissive epigenetic environment that supports stem-like properties, therapy resistance, and relapse. In addition to its canonical catalytic role, KMT2A influences chromatin remodeling, enhancer-promoter communication, and transcriptional memory, all of which are crucial for maintaining stemness and enabling cancer cell reprogramming. Given its multifaceted role in cancer and stem cell biology, KMT2A is a promising therapeutic target, and inhibitors that disrupt its interactions, enzymatic activity, or fusion pathways are showing encouraging results. Moreover, current clinical trials investigating venetoclax and menin inhibitors offer renewed hope for curative therapies. This review summarizes the current understanding of the transcriptional mechanisms and noncatalytic roles of KMT2A and the translational implications of targeting KMT2A-driven pathways in stemness and cancer, paving the way for advanced therapeutic intervention.

Indexed as

Gene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseMyeloid-Lymphoid Leukemia ProteinNeoplasmsNeoplastic Stem CellsAnimalsEpigenesis, GeneticHumansTranscription, GeneticHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinEpigenetic regulationKMT2AOncogenesisStemness and differentiationTherapeutic targeting

Identifiers

PMID41441935

What OpenQuestion holds

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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.