ArticleNature communications2017
Alu-dependent RNA editing of GLI1 promotes malignant regeneration in multiple myeloma.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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.
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Who cites it
83 citing papers in PubMed, 141 citations in OpenAlex.
- 8-Chloroadenosine suppresses hepatocellular carcinoma progression via ADAR1/PPARγ axis-mediated lipid metabolism.Genes & diseases · 2026Article
- Proteomic profiling revealed unique disease biology associated with 1q abnormalities in multiple myeloma.NPJ precision oncology · 2026Article
- TSniffer: unbiased de novo identification of RNA editing sites and quantification of editing activity in RNA-seq data.Genome biology · 2026Article
- RNA editing: an emerging frontier in cancer therapy - explorations, opportunities, and challenges.International journal of surgery (London, England) · 2026Article
- Nanobioreactor detection of space-associated hematopoietic stem and progenitor cell aging.Cell stem cell · 2025Article
- Alu RNA pseudoknot alterations influence SRP9/SRP14 association.RNA (New York, N.Y.) · 2025Article
- ADARs: pleiotropy in function, versatility in application.Nucleic acids research · 2025Review
- Adenosine-to-inosine RNA editing in cancer: molecular mechanisms and downstream targets.Protein & cell · 2025Review
- Resistance to immunomodulatory drugs in multiple myeloma: the cereblon pathway and beyond.Haematologica · 2025Review
- ADAR1-high tumor-associated macrophages induce drug resistance and are therapeutic targets in colorectal cancer.Molecular cancer · 2025Article
- Article
- EZH2 serves as a viable therapeutic target for myeloma-induced osteolytic bone destruction.Nature communications · 2025Article
- ADARp110 promotes hepatocellular carcinoma progression via stabilization of CD24 mRNA.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of RNA modifications in blood development and regeneration.Experimental hematology · 2024Review
- Detecting haplotype-specific transcript variation in long reads with FLAIR2.Genome biology · 2024Article
- Review
- Malignant A-to-I RNA editing by ADAR1 drives T cell acute lymphoblastic leukemia relapse via attenuating dsRNA sensing.Cell reports · 2024Article
- The Genetic and Molecular Drivers of Multiple Myeloma: Current Insights, Clinical Implications, and the Path Forward.Pharmacogenomics and personalized medicine · 2024Review
- RNA Editing in Cancer Progression.Cancers · 2023Review
- Stem-Cell Aging and Pathways to Precancer Evolution.The New England journal of medicine · 2023Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Despite novel therapies, relapse of multiple myeloma (MM) is virtually inevitable. Amplification of chromosome 1q, which harbors the inflammation-responsive RNA editase adenosine deaminase acting on RNA (ADAR)1 gene, occurs in 30-50% of MM patients and portends a poor prognosis. Since adenosine-to-inosine RNA editing has recently emerged as a driver of cancer progression, genomic amplification combined with inflammatory cytokine activation of ADAR1 could stimulate MM progression and therapeutic resistance. Here, we report that high ADAR1 RNA expression correlates with reduced patient survival rates in the MMRF CoMMpass data set. Expression of wild-type, but not mutant, ADAR1 enhances Alu-dependent editing and transcriptional activity of GLI1, a Hedgehog (Hh) pathway transcriptional activator and self-renewal agonist, and promotes immunomodulatory drug resistance in vitro. Finally, ADAR1 knockdown reduces regeneration of high-risk MM in serially transplantable patient-derived xenografts. These data demonstrate that ADAR1 promotes malignant regeneration of MM and if selectively inhibited may obviate progression and relapse.
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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.