ReviewBiology2021
Histone H3K4 Methyltransferases as Targets for Drug-Resistant Cancers.
Review in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Mutations in histone lysine methyltransferase genes are associated with autoimmune cytopenias: a single-center study.Blood vessels, thrombosis & hemostasis · 2026Article
- HPV-Driven Cervical Carcinogenesis: Genetic and Epigenetic Mechanisms and Diagnostic Approaches.International journal of molecular sciences · 2026Review
- Expression of ubiquitin carboxyl-terminal hydrolase isozyme L1 and chromogranin A regulated via histone-modification through Rho/ERK/NFκB signaling in oxaliplatin-resistant colorectal cancer cells.International journal of medical sciences · 2026Article
- Menin-driven mTOR signaling sustains taxane resistance in CRPC and reveals a targetable vulnerability for combination therapy.Cell communication and signaling : CCS · 2025Article
- Expression profiles of histone H4K20 methylation and its associated enzymes in mouse cardiac disease and human heart failure.Epigenetics · 2025Article
- A histone-centric multi-omics study shows that increased H3K4 methylation sustains triple-negative breast cancer phenotypes.Nature communications · 2025Article
- Precision epigenetic therapies in oncology.Cancer metastasis reviews · 2025Review
- Epigenetic modifications in early stage lung cancer: pathogenesis, biomarkers, and early diagnosis.MedComm · 2025Review
- Epigenetic insights into prostate cancer: exploring histone modifications and their therapeutic implications.Frontiers in oncology · 2025Review
- Histone lysine methylation modifiers controlled by protein stability.Experimental & molecular medicine · 2024Review
- ZNF8 Orchestrates with Smad3 to Promote Lung Metastasis by Recruiting SMYD3 in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Insights into the mechanisms driven by H3K4 KMTs in pancreatic cancer.The Biochemical journal · 2024Review
- MLL1 regulates cytokine-driven cell migration and metastasis.Science advances · 2024Article
- Revealing role of epigenetic modifiers and DNA oxidation in cell-autonomous regulation of Cancer stem cells.Cell communication and signaling : CCS · 2024Article
- Lysine Methyltransferase EhPKMT2 Is Involved in the In Vitro Virulence ofPathogens (Basel, Switzerland) · 2023Article
- Targeting Epigenetic Changes Mediated by Members of the SMYD Family of Lysine Methyltransferases.Molecules (Basel, Switzerland) · 2023Review
- H3 histone methylation landscape in male urogenital cancers: from molecular mechanisms to epigenetic biomarkers and therapeutic targets.Frontiers in cell and developmental biology · 2023Review
- New perspectives on epigenetic modifications and PARP inhibitor resistance in HR-deficient cancers.Cancer drug resistance (Alhambra, Calif.) · 2023Article
- Transcriptional regulation of macrophages in heart failure.Frontiers in cardiovascular medicine · 2023Review
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 2 institutions in 2 countries.
Funding
Abstract
The KMT2 (MLL) family of proteins, including the major histone H3K4 methyltransferase found in mammals, exists as large complexes with common subunit proteins and exhibits enzymatic activity. SMYD, another H3K4 methyltransferase, and SET7/9 proteins catalyze the methylation of several non-histone targets, in addition to histone H3K4 residues. Despite these structural and functional commonalities, H3K4 methyltransferase proteins have specificity for their target genes and play a role in the development of various cancers as well as in drug resistance. In this review, we examine the overall role of histone H3K4 methyltransferase in the development of various cancers and in the progression of drug resistance. Compounds that inhibit protein-protein interactions between KMT2 family proteins and their common subunits or the activity of SMYD and SET7/9 are continuously being developed for the treatment of acute leukemia, triple-negative breast cancer, and castration-resistant prostate cancer. These H3K4 methyltransferase inhibitors, either alone or in combination with other drugs, are expected to play a role in overcoming drug resistance in leukemia and various solid cancers.
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What Socratic 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 Socratic graph.