ArticleScientific reports2016
Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Epigenetic regulation of major histocompatibility complexes in gastrointestinal malignancies and the potential for clinical interception.Clinical epigenetics · 2024Pooled it
- Advancing Treatment Options for Merkel Cell Carcinoma: A Review of Tumor-Targeted Therapies.International journal of molecular sciences · 2024Review
- Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling.PLoS pathogens · 2024Article
- Merkel Cell Carcinoma: Integrating Epidemiology, Immunology, and Therapeutic Updates.American journal of clinical dermatology · 2024Review
- Merkel cell carcinoma: updates in tumor biology, emerging therapies, and preclinical models.Frontiers in oncology · 2024Review
- Insights into anti-tumor immunityFrontiers in immunology · 2023Review
- Article
- T-Cell Mediated Immunity in Merkel Cell Carcinoma.Cancers · 2022Review
- Genomic evidence suggests that cutaneous neuroendocrine carcinomas can arise from squamous dysplastic precursors.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- Untargeted Metabolomics Showed Accumulation of One-Carbon Metabolites to Facilitate DNA Methylation during Extracellular Matrix Detachment of Cancer Cells.Metabolites · 2022Article
- Viral Status Predicts the Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma.The Journal of investigative dermatology · 2022Article
- HDAC2 Is Involved in the Regulation of BRN3A in Melanocytes and Melanoma.International journal of molecular sciences · 2022Article
- Circulating Tumor Cells: Does Ion Transport Contribute to Intravascular Survival, Adhesion, Extravasation, and Metastatic Organotropism?Reviews of physiology, biochemistry and pharmacology · 2022Review
- The histone deacetylase inhibitor M344 as a multifaceted therapy for pancreatic cancer.PloS one · 2022Article
- The Role of Histone Post-Translational Modifications in Merkel Cell Carcinoma.Frontiers in oncology · 2022Review
- Epigenetic Dysregulations in Merkel Cell Polyomavirus-Driven Merkel Cell Carcinoma.International journal of molecular sciences · 2021Review
- Characterizing DNA methylation signatures and their potential functional roles in Merkel cell carcinoma.Genome medicine · 2021Article
- Quality Is King: Fundamental Insights into Tumor Antigenicity from Virus-Associated Merkel Cell Carcinoma.The Journal of investigative dermatology · 2021Review
- Review
- Merkel Cell Carcinoma from Molecular Pathology to Novel Therapies.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors in situ and are completely absent on MCC cell lines in vitro. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both in vitro and in vivo. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.
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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.