ArticleProtein & cell2014
Driver mutations of cancer epigenomes.
Article in Protein & cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- Genetic alterations of histone lysine methyltransferases and their significance in breast cancer.Oncotarget · 2015Pooled it
- Trial
- Viral mimicry escape as a necessary feature of malignant transformation.Nature reviews. Cancer · 2026Review
- The conserved N-terminal SANT1-binding domain (SBD) of EZH2 regulates PRC2 activity.Genes & development · 2026Article
- Rare KDM4C variants and reduced expression underlie epigenetic dysregulation in rheumatoid arthritis.Immunologic research · 2026Article
- Article
- Assessing the selective impact of histone modifying drugs on adenoid cystic carcinoma cells and their stem cell counterparts.BMC cancer · 2025Article
- Comprehensive Analysis of Human Colorectal Cancers Harboring Polymerase Epsilon Mutations.International journal of molecular sciences · 2025Article
- NAT10-mediated mRNA NNature cell biology · 2024Article
- Combining evolution and protein language models for an interpretable cancer driver mutation prediction with D2Deep.Briefings in bioinformatics · 2024Article
- Cancer-associated Histone H3 N-terminal arginine mutations disrupt PRC2 activity and impair differentiation.Nature communications · 2024Article
- The Histone Deacetylase Family: Structural Features and Application of Combined Computational Methods.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Cancer cell plasticity: from cellular, molecular, and genetic mechanisms to tumor heterogeneity and drug resistance.Cancer metastasis reviews · 2024Review
- Pairwise and higher-order epistatic effects among somatic cancer mutations across oncogenesis.Mathematical biosciences · 2023Article
- Alterations in the Epigenetic Machinery Associated with Prostate Cancer Health Disparities.Cancers · 2023Article
- The role of chromatin remodeler SMARCA4/BRG1 in brain cancers: a potential therapeutic target.Oncogene · 2023Review
- Harnessing Epigenetics for Breast Cancer Therapy: The Role of DNA Methylation, Histone Modifications, and MicroRNA.International journal of molecular sciences · 2023Review
- Article
- The function of histone methylation and acetylation regulators in GBM pathophysiology.Frontiers in oncology · 2023Review
- New Insights into SARS-CoV-2 and Cancer Cross-Talk: Does a Novel Oncogenesis Driver Emerge?Vaccines · 2022Review
24 more citing papers are in PubMed but not listed here.
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
Epigenetic alterations are associated with all aspects of cancer, from tumor initiation to cancer progression and metastasis. It is now well understood that both losses and gains of DNA methylation as well as altered chromatin organization contribute significantly to cancer-associated phenotypes. More recently, new sequencing technologies have allowed the identification of driver mutations in epigenetic regulators, providing a mechanistic link between the cancer epigenome and genetic alterations. Oncogenic activating mutations are now known to occur in a number of epigenetic modifiers (i.e. IDH1/2, EZH2, DNMT3A), pinpointing epigenetic pathways that are involved in tumorigenesis. Similarly, investigations into the role of inactivating mutations in chromatin modifiers (i.e. KDM6A, CREBBP/EP300, SMARCB1) implicate many of these genes as tumor suppressors. Intriguingly, a number of neoplasms are defined by a plethora of mutations in epigenetic regulators, including renal, bladder, and adenoid cystic carcinomas. Particularly striking is the discovery of frequent histone H3.3 mutations in pediatric glioma, a particularly aggressive neoplasm that has long remained poorly understood. Cancer epigenetics is a relatively new, promising frontier with much potential for improving cancer outcomes. Already, therapies such as 5-azacytidine and decitabine have proven that targeting epigenetic alterations in cancer can lead to tangible benefits. Understanding how genetic alterations give rise to the cancer epigenome will offer new possibilities for developing better prognostic and therapeutic strategies.
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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.