ReviewGenes2018
ADAR1 Editing and its Role in Cancer.
Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Meta-Analysis of Keratoconus Transcriptomic Data Revealed Altered RNA Editing Levels Impacting Keratin Genomic Clusters.Investigative ophthalmology & visual science · 2023Pooled it
- ADAR1-circRAB5A-BIP axis governs radiotherapy resistance in colorectal cancer through coordinating protective autophagy and apoptosis.Cancer biology & therapy · 2026Article
- ADAR-mediated RNA editing in CNS disorders: from pathogenic mechanisms to therapeutic opportunities.Cellular & molecular biology letters · 2026Review
- The regulatory mechanism and clinical significance of RNA editing in prostate cancer.Current urology · 2026Review
- Review
- Molecular Context of ADAR-Mediated Editing of Coding RNA in Colorectal and Lung Cancers.International journal of molecular sciences · 2026Article
- Heterologous expression of Pinus massoniana VNS2 enhances secondary cell wall deposition in poplar.Plant cell reports · 2026Article
- ADAR1 expression in different cancer cell lines and its change under heat shock.Journal of applied genetics · 2025Article
- Expression Profile and Clinical Relevance of ADAR Family Genes in Head and Neck Squamous Cell Carcinoma.Genes · 2025Article
- Intracellular Mis-Localization of Modified RNA Molecules and Non-Coding RNAs: Facts from Hematologic Malignancies.Current issues in molecular biology · 2025Review
- Nomogram Based on A-To-I RNA Editing for Predicting Overall Survival in Patients With Breast Cancer.Journal of cellular and molecular medicine · 2025Article
- Adenosine-to-inosine RNA editing in cancer: molecular mechanisms and downstream targets.Protein & cell · 2025Review
- Clinical and Prognostic Implications of an Alternative Splicing-related Risk Model Based on TP53 Status in Breast Cancer.Current pharmaceutical biotechnology · 2025Article
- ADAR3 modulates neuronal differentiation and regulates mRNA stability and translation.Nucleic acids research · 2024Article
- Structurally Specific Z-DNA Proteolysis Targeting Chimera Enables Targeted Degradation of Adenosine Deaminase Acting on RNA 1.Journal of the American Chemical Society · 2024Article
- Malignant A-to-I RNA editing by ADAR1 drives T cell acute lymphoblastic leukemia relapse via attenuating dsRNA sensing.Cell reports · 2024Article
- Harnessing ADAR-Mediated Site-Specific RNA Editing in Immune-Related Disease: Prediction and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Genetically engineered nanovesicles mobilize synergistic antitumor immunity by ADAR1 silence and PDL1 blockade.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Biological roles of A-to-I editing: implications in innate immunity, cell death, and cancer immunotherapy.Journal of experimental & clinical cancer research : CR · 2023Review
- ADAR1-mediated RNA editing promotes B cell lymphomagenesis.iScience · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
It is well established that somatic mutations and escape of immune disruption are two essential factors in cancer initiation and progression. With an increasing number of second-generation sequencing data, transcriptomic modifications, so called RNA mutations, are emerging as significant forces that drive the transition from normal cell to malignant tumor, as well as providing tumor diversity to escape an immune attack. Editing of adenosine to inosine (A-to-I) in double-stranded RNA, catalyzed by adenosine deaminases acting on RNA (ADARs), is one dynamic modification that in a combinatorial manner can give rise to a very diverse transcriptome. Since the cell interprets inosine as guanosine (G), A-to-I editing can result in non-synonymous codon changes in transcripts as well as yield alternative splicing, but also affect targeting and disrupt maturation of microRNAs. ADAR-mediated RNA editing is essential for survival in mammals, however, its dysregulation causes aberrant editing of its targets that may lead to cancer. ADAR1 is commonly overexpressed, for instance in breast, lung, liver and esophageal cancer as well as in chronic myelogenous leukemia, where it promotes cancer progression. It is well known that ADAR1 regulates type I interferon (IFN) and its induced gene signature, which are known to operate as a significant barrier to tumor formation and progression. Adding to the complexity, ADAR1 expression is also regulated by IFN. In this review, we discussed the regulatory mechanisms of ADAR1 during tumorigenesis through aberrant editing of specific substrates. Additionally, we hypothesized that elevated ADAR1 levels play a role in suppressing an innate immunity response in cancer cells.
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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.