ReviewMolecular therapy. Oncology2024
Genetic dysregulation of EP300 in cancers in light of cancer epigenome control - targeting of p300-proficient and -deficient cancers.
Review in Molecular therapy. Oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Determination of copy number variations and affected gene networks in breast cancer.Biomedical reports · 2026Article
- UniversalEPI: robust prediction of cell type-specific and differential chromatin interactions from DNA sequence and chromatin accessibility.Nucleic acids research · 2026Article
- Molecular and clinical disparity ofTranslational lung cancer research · 2026Article
- Adaptive introgression shaping genomic adaptation and ancestral mosaicism of Changthangi sheep for high-altitude survival and pashmina excellence.BMC genomics · 2026Article
- Dynamic crotonylation of Bub3 regulates mitotic checkpoint silencing and chromosome segregation.Journal of molecular cell biology · 2026Article
- Ultrarare Variants in DNA Damage Repair and Mitochondrial Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome and Acute Behavioral Regression in Neurodevelopmental Disorders.Developmental neuroscience · 2026Article
- Metastatic progression of pheochromocytoma and paraganglioma occurs via parallel evolution.NPJ precision oncology · 2026Article
- Multi-omic integration identifies broad drug resistance mechanisms and strategies to therapeutically reprogram cancer cells.iScience · 2026Article
- EP300 promotes bladder cancer cell migration through SNAI2.PloS one · 2026Article
- HIF1A, BRG1, and p300 interaction confers paclitaxel-induced drug resistance by enabling the overexpression ofMolecular therapy. Oncology · 2025Article
- EP300 deficiency leads to chronic replication stress mediated by defective replication fork protection.Nature communications · 2025Article
- Mutations in CREBBP and EP300 HAT and Bromo Domains Drive Hypermutation and Predict Survival in GI Cancers Treated with Immunotherapy.Biomedicines · 2025Article
- Expression Analysis of miR-519a-3p and miR-379-5p in Colorectal Cancer Patients: A Combined Experimental and Bioinformatic Approach.Diagnostics (Basel, Switzerland) · 2025Article
- Decoding Molecular Interactions: Unraveling the Crosstalk between the Wnt Pathway and Key Signaling Networks by miRNA in Colorectal Cancer Progression.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Targeting inflammation in cancer therapy: from mechanistic insights to emerging therapeutic approaches.Journal of translational medicine · 2025Review
- Machine learning explores the prognostic and immuno-oncological impact of mitochondrial unfolded protein response in CESC.Discover oncology · 2025Article
- A Case of False-Negative Results in the One-Step Nucleic Acid Amplification Assay for Sentinel Lymph Node Metastasis in Breast Cancer with Low Cytokeratin 19 Expression.Case reports in oncologyArticle
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some cancer types including bladder, cervical, and uterine cancers are characterized by frequent mutations in EP300 that encode histone acetyltransferase p300. This enzyme can act both as a tumor suppressor and oncogene. In this review, we describe the role of p300 in cancer initiation and progression regarding EP300 aberrations that have been identified in TGCA Pan-Cancer Atlas studies and we also discuss possible anticancer strategies that target EP300 mutated cancers. Copy number alterations, truncating mutations, and abnormal EP300 transcriptions that affect p300 abundance and activity are associated with several pathological features such as tumor grading, metastases, and patient survival. Elevated EP300 correlates with a higher mRNA level of other epigenetic factors and chromatin remodeling enzymes that co-operate with p300 in creating permissive conditions for malignant transformation, tumor growth and metastases. The status of EP300 expression can be considered as a prognostic marker for anticancer immunotherapy efficacy, as EP300 mutations are followed by an increased expression of PDL-1.HAT activators such as CTB or YF2 can be applied for p300-deficient patients, whereas the natural and synthetic inhibitors of p300 activity, as well as dual HAT/bromodomain inhibitors and the PROTAC degradation of p300, may serve as strategies in the fight against p300-fueled cancers.
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