ReviewEpigenetics & chromatin2018
KDM1A microenvironment, its oncogenic potential, and therapeutic significance.
Review in Epigenetics & chromatin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 87 citations in OpenAlex.
- RAF1 Promotes Gstt1-Mediated Ferroptosis by Promoting KDM1A Recruitment to Facilitate Pilocarpine-Induced Acute Seizure-Associated Neuronal Injury.CNS neuroscience & therapeutics · 2026Article
- Review
- Histone demethylase inhibitors: developmental insights and current status.Future medicinal chemistry · 2025Review
- Epigenomic Modulators and Thyroid Hormone Receptor β Agonists: A New Paradigm for Tumor Suppression in Thyroid Cancer.Endocrinology · 2025Review
- Construction of a Prognostic Model Using RNA Processing Factor Genes and the Key Role of NSUN6 in Glioma Outcomes.Journal of cellular and molecular medicine · 2025Article
- Current advances and future directions in targeting histone demethylases for cancer therapy.Molecules and cells · 2025Review
- REST missense mutations reveal disrupted Re1 motif binding and co-repressor interactions in uterine fibroids.Frontiers in bioinformatics · 2025Article
- GSTRPCA: irregular tensor singular value decomposition for single-cell multi-omics data clustering.Briefings in bioinformatics · 2024Article
- KDM1A, a potent and selective target, for the treatment of DNMT3A-deficient non-small cell lung cancer.British journal of cancer · 2024Article
- Article
- Kdm1a safeguards the topological boundaries of PRC2-repressed genes and prevents aging-related euchromatinization in neurons.Nature communications · 2024Article
- Pioneer factor Pax7 initiates two-step cell-cycle-dependent chromatin opening.Nature structural & molecular biology · 2024Article
- Article
- Apigenin as an emerging hepatoprotective agent: current status and future perspectives.Frontiers in pharmacology · 2024Review
- Article
- The First Pituitary Proteome Landscape From Matched Anterior and Posterior Lobes for a Better Understanding of the Pituitary Gland.Molecular & cellular proteomics : MCP · 2023Article
- Review
- Molecular Characterization and Clinical Relevance of NFrontiers in oncology · 2022Article
- Article
- KDM1A inhibition augments the efficacy of rapamycin for the treatment of endometrial cancer.Cancer letters · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The lysine-specific histone demethylase 1A (KDM1A) was the first demethylase to challenge the concept of the irreversible nature of methylation marks. KDM1A, containing a flavin adenine dinucleotide (FAD)-dependent amine oxidase domain, demethylates histone 3 lysine 4 and histone 3 lysine 9 (H3K4me1/2 and H3K9me1/2). It has emerged as an epigenetic developmental regulator and was shown to be involved in carcinogenesis. The functional diversity of KDM1A originates from its complex structure and interactions with transcription factors, promoters, enhancers, oncoproteins, and tumor-associated genes (tumor suppressors and activators). In this review, we discuss the microenvironment of KDM1A in cancer progression that enables this protein to activate or repress target gene expression, thus making it an important epigenetic modifier that regulates the growth and differentiation potential of cells. A detailed analysis of the mechanisms underlying the interactions between KDM1A and the associated complexes will help to improve our understanding of epigenetic regulation, which may enable the discovery of more effective anticancer drugs.
Indexed as
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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.