ReviewClinical epigenetics2025
Multiple functions of the lysine methyltransferase KMT5a in cancer: potential targets for innovative therapies.
Review in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed.
- The lysine methyltransferase KMT5a and p53 regulate the expression of the key autophagy adaptor p62/SQSTM1 in glioblastoma.Cell communication and signaling : CCS · 2026Article
- Nanopore and EPIC array profiling unmask an atypical non-midline H3 K27-altered glioma: a case report.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Lysine methyltransferase 5a (KMT5a) plays a key role in the pathogenesis of many human diseases. Here, we review the diverse impacts of KMT5a activity on human cancer development and progression. First, KMT5a is the only Mammalian enzyme that specifically induces monomethylation of histone 4 (H4) on lysine 20, thus regulating chromatin organization and, in turn, the transcription of several oncogenes and tumor suppressor genes. KMT5a, by inducing H4 methylation, also critically establishes the choice between different pathways of DNA double-strand break repair, with important consequences for genomic instability and cancer origin. Finally, KMT5a also methylates lysine residues on nonhistone proteins, and KMT5a-induced methylation of key oncogenic and tumor suppressor proteins, including TP53, strongly affects cancer cell functions. Overall, KMT5a is overexpressed in a high percentage and wide variety of human cancers and has protumorigenic activity, which makes it a target for innovative therapy.
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Registered trials
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.