ReviewAdvances in cancer research2016
H3K27 Methylation: A Focal Point of Epigenetic Deregulation in Cancer.
Review in Advances in cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 64 citations in OpenAlex.
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
- Defining the heterogeneous molecular landscape of lung cancer cell responses to epigenetic inhibition.Communications biology · 2026Article
- A metabolomics approach to target the effect of histone protein methyltransferase-specific probe UNC1999 on cryptic metabolites in an endophytic fungusFrontiers in microbiology · 2026Article
- Lytic or Latent Phase in Human Cytomegalovirus Infection: An Epigenetic Trigger.International journal of molecular sciences · 2025Review
- Review
- Prominent fibroblast growth factor 21 with less abundant tumor-associated macrophages in hepatic mass of the conditional mgmt-deleted mice using LysM-Cre system.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Review
- Antisense-mediated exon skipping targeting EZH2 suppresses tumor growth in a xenograft mouse model of hepatocellular carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The janus-faced biology of GPNMB: from tissue homeostasis to cancer pathogenesis.Frontiers in molecular biosciences · 2025Review
- Decoding bronchopulmonary dysplasia in premature infants through an epigenetic lens.Frontiers in medicine · 2025Review
- Epigenetic alterations and advancement of lymphoma treatment.Annals of hematology · 2024Review
- Epigenetic insights into Fragile X Syndrome.Frontiers in cell and developmental biology · 2024Review
- Article
- Less Severe Polymicrobial Sepsis in ConditionalInternational journal of molecular sciences · 2023Article
- Less Severe Lipopolysaccharide-Induced Inflammation in ConditionalInternational journal of molecular sciences · 2023Article
- Less Severe Sepsis in Cecal Ligation and Puncture Models with and without Lipopolysaccharide in Mice with ConditionalInternational journal of molecular sciences · 2023Article
- The Regulatory Roles ofInternational journal of molecular sciences · 2023Article
- Direct assessment of histone function using histone replacement.Trends in biochemical sciences · 2023Review
- Diffuse Intrinsic Pontine Glioma: Molecular Landscape, Evolving Treatment Strategies and Emerging Clinical Trials.Journal of personalized medicine · 2022Review
- Epigenetic Determinants of Racial Disparity in Breast Cancer: Looking beyond Genetic Alterations.Cancers · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Epigenetics, the modification of chromatin without changing the DNA sequence itself, determines whether a gene is expressed, and how much of a gene is expressed. Methylation of lysine 27 on histone 3 (H3K27me), a modification usually associated with gene repression, has established roles in regulating the expression of genes involved in lineage commitment and differentiation. Not surprisingly, alterations in the homeostasis of this critical mark have emerged as a recurrent theme in the pathogenesis of many cancers. Perturbations in the distribution or levels of H3K27me occur due to deregulation at all levels of the process, either by mutation in the histone itself, or changes in the activity of the writers, erasers, or readers of this mark. Additionally, as no single histone mark alone determines the overall transcriptional readiness of a chromatin region, deregulation of other chromatin marks can also have dramatic consequences. Finally, the significance of mutations altering H3K27me is highlighted by the poor clinical outcome of patients whose tumors harbor such lesions. Current therapeutic approaches targeting aberrant H3K27 methylation remain to be proven useful in the clinic. Understanding the biological consequences and gene expression pathways affected by aberrant H3K27 methylation may lead to identification of new therapeutic targets and strategies.
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.