ReviewOncotarget2021
Cancer-epigenetic function of the histone methyltransferase KMT2D and therapeutic opportunities for the treatment of KMT2D-deficient tumors.
Review in Oncotarget, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Pooled it
- HIRA loss is frequent but not universal in human fumarate hydratase-deficient renal cell carcinoma and defines divergent oncogenic programs.Biomarker research · 2026Article
- Histone methyltransferase KMT2D promotes castration-resistant prostate cancer progression by reactivating AR through FOXA1.Oncogene · 2026Article
- Review
- A tryptophan-phenylalanine binding motif for the histone methyltransferases MLL4 and MLL3.The Journal of biological chemistry · 2026Article
- OncoBERT: Context-Aware Modeling of Somatic Mutations for Precision Oncology.bioRxiv : the preprint server for biology · 2026Article
- Radiographically occult bone marrow metastasis in relapsed small cell lung cancer presenting with rapidly progressive thrombocytopenia: a case report.Frontiers in oncology · 2026Article
- Genomic Characteristics of Bladder Cancer: An AACR Project GENIE Study.International journal of molecular sciences · 2025Article
- Histone methyltransferase KMT2D targets the SPOP-G3BP1 axis to enhance AR stability and drive castration-resistant prostate cancer progression.Molecular biomedicine · 2025Article
- Genomic and Demographic Characteristics of Angiosarcoma as Described in the AACR Project GENIE Registry.Cancers · 2025Article
- Descriptive Genomic Analysis of Ampullary Carcinoma Utilizing the AACR Project GENIE Dataset.Current issues in molecular biology · 2025Article
- Role of Genes in Dens Invaginatus: A Whole Exome Sequencing Study.International journal of clinical pediatric dentistry · 2025Article
- Actionable Genes and Carcinogenic Pathways for Gastric Cancer in Latinos.Cancer medicine · 2025Article
- Advancing Medulloblastoma Therapy in Pediatrics: Integrative Molecular Classification and Emerging Treatments.Brain sciences · 2025Review
- Whole genome sequencing and single-cell transcriptomics identify KMT2D inactivation as a potential new driver for pituitary tumors: a case report.BJC reports · 2025Article
- Wnt/β-catenin activation by mutually exclusive FBXW11 and CTNNB1 hotspot mutations drives salivary basal cell adenoma.Nature communications · 2025Article
- Article
- Coding Variants of the Genitourinary Development GeneJCO precision oncology · 2025Article
- Role of histone-lysine N-methyltransferase 2D (KMT2D) in MEK-ERK signaling-mediated epigenetic regulation: a phosphoproteomics perspective.Frontiers in bioinformatics · 2025Article
- Case Report: Genomic characterization of a rare skull-base plasmacytoma.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Epigenetic mechanisms are central to understanding the molecular basis underlying tumorigenesis. Aberrations in epigenetic modifiers alter epigenomic landscapes and play a critical role in tumorigenesis. Notably, the histone lysine methyltransferase KMT2D (a COMPASS/ Set1 family member; also known as MLL4, ALR, and MLL2) is among the most frequently mutated genes in many different types of cancer. Recent studies have demonstrated how KMT2D loss induces abnormal epigenomic reprograming and rewires molecular pathways during tumorigenesis. These findings also have clinical and therapeutic implications for cancer treatment. In this review, we summarize recent advances in understanding the role of KMT2D in regulating tumorigenesis and discuss therapeutic opportunities for the treatment of KMT2D-deficient tumors.
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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.