ReviewBiomolecules & therapeutics2025
DOT1L as a Therapeutic Target: Insights into Epigenetic Regulation and Cancer Treatment.
Review in Biomolecules & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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
3 citing papers in PubMed.
- Review
- Post-translational modifications in retinoblastoma: mechanisms, immune regulation, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Transcriptomic Profiling Identifies Higher DOT1L Expression as a Candidate Biomarker for a Positive Response to Gemcitabine in Cholangiocarcinoma.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruptor of Telomeric Silencing 1-Like (DOT1L) has emerged as a critical epigenetic regulator in cancer, primarily because of its role as the sole histone methyltransferase responsible for histone H3 at lysine 79 methylation. This modification affects transcriptional activation, DNA repair, and cell cycle progression. Its dysregulation is associated with both hematological and solid tumors. In Mixed-lineage leukemia (MLL)-rearranged leukemia, DOT1L maintains aberrant gene expression patterns at loci such as HOXA and MEIS1, supporting leukemic stem cell survival and driving oncogenesis. In solid tumors, DOT1L influences diverse processes, including epithelial-mesenchymal transition, angiogenesis, and cell cycle regulation, contributing to tumor growth and metastasis. Therapeutic strategies targeting DOT1L using inhibitors, such as EPZ-5676, have shown promise in preclinical and clinical studies, highlighting their potential as versatile targets for precision oncology. This review summarizes the recent findings on DOT1L's involvement in cancer development and its potential as a therapeutic target.
Indexed as
Identifiers
What OpenQuestion holds
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.