ReviewFuture medicinal chemistry2016
H3K36 methyltransferases as cancer drug targets: rationale and perspectives for inhibitor development.
Review in Future medicinal chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled 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.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Role of Ash1l in Tourette syndrome and other neurodevelopmental disorders.Developmental neurobiology · 2021Pooled it
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.Nucleic acids research · 2026Article
- Regulation of the histone H3K36 methyltransferase Set2 by the histone chaperone Spt6.bioRxiv : the preprint server for biology · 2026Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Structure-Based Development of Novel Spiro-Piperidine ASH1L Inhibitors.Journal of medicinal chemistry · 2025Article
- Thioamides in medicinal chemistry and as small molecule therapeutic agents.European journal of medicinal chemistry · 2024Review
- Disruption of H3K36 methylation provokes cellular plasticity to drive aberrant glandular formation and squamous carcinogenesis.Developmental cell · 2024Article
- Alpha Satellite DNA in Targeted Drug Therapy for Prostate Cancer.International journal of molecular sciences · 2023Article
- Epigenetic regulation of SMAD3 by histone methyltransferase SMYD2 promotes lung cancer metastasis.Experimental & molecular medicine · 2023Article
- Target validation and structure-based virtual screening to Discover potential lead molecules against the oncogenic NSD1 histone methyltransferase.In silico pharmacology · 2023Article
- SETD2-H3K36ME3: an important bridge between the environment and tumors.Frontiers in genetics · 2023Review
- Review
- NSD2 as a Promising Target in Hematological Disorders.International journal of molecular sciences · 2022Review
- Structural and functional specificity of H3K36 methylation.Epigenetics & chromatin · 2022Review
- The role of NSD1, NSD2, and NSD3 histone methyltransferases in solid tumors.Cellular and molecular life sciences : CMLS · 2022Review
- Expression pattern and regulatory effect of lysine-specific demethylase 2A gene in clear cell renal cell carcinoma.BMC urology · 2021Article
- Discovery of first-in-class inhibitors of ASH1L histone methyltransferase with anti-leukemic activity.Nature communications · 2021Article
- Downregulation of METTL7B Inhibits Proliferation of Human Clear Cell Renal Cancer CellsFrontiers in oncology · 2021Article
- Loss of Function SETD2 Mutations in Poorly Differentiated Metastases from Two Hürthle Cell Carcinomas of the Thyroid.Cancers · 2020Article
- H3K9me3, H3K36me3, and H4K20me3 Expression Correlates with Patient Outcome in Esophageal Squamous Cell Carcinoma as Epigenetic Markers.Digestive diseases and sciences · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Methylation at histone 3, lysine 36 (H3K36) is a conserved epigenetic mark regulating gene transcription, alternative splicing and DNA repair. Genes encoding H3K36 methyltransferases (KMTases) are commonly overexpressed, mutated or involved in chromosomal translocations in cancer. Molecular biology studies have demonstrated that H3K36 KMTases regulate oncogenic transcriptional programs. Structural studies of the catalytic SET domain of H3K36 KMTases have revealed intriguing opportunities for design of small molecule inhibitors. Nevertheless, potent inhibitors for most H3K36 KMTases have not yet been developed, underlining the challenges associated with this target class. As we now have strong evidence linking H3K36 KMTases to cancer, drug development efforts are predicted to yield novel compounds in the near future.
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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.