ArticleCell reports2024
Small-molecule inhibition of the METTL3/METTL14 complex suppresses neuroblastoma tumor growth and promotes differentiation.
Article in Cell reports, 2024. 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, 33 citations in OpenAlex.
- Article
- Virtual screening and experimental validation of a METTL3-targeting peptide withJournal of enzyme inhibition and medicinal chemistry · 2026Article
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- The Role of NMedComm · 2026Review
- METTL3-mediated mJournal of translational medicine · 2026Article
- RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition.Cell death & disease · 2026Article
- Epigenetic regulation in cancer metastasis.Discover oncology · 2026Review
- Hepatocyte Mettl3 Deficiency Drives Primary Sclerosing Cholangitis and Liver Fibrosis via Cholangiocyte-Macrophage Crosstalk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epitranscriptomic Regulation of Platinum Resistance via the METTL3-ADAM23 Axis in Ovarian Cancer.Cells · 2026Article
- Advances in multi-omics research on neuroblastoma.Frontiers in pediatrics · 2026Review
- m6A-Targeted Cancer Therapy: Molecular Targets, Inhibitors, and Nanodelivery Strategies.International journal of nanomedicine · 2026Review
- mRNA processing in cancer immunotherapy: emerging targets, resistance mechanisms, and therapeutic opportunities.Frontiers in immunology · 2026Review
- The METTL3-YTHDC1 axis mediates architectural RNA mMolecular cancer · 2025Article
- Deciphering the interplay between SETD2 mediated H3K36me3 and RNA N6-methyladenosine in clear cell renal cell carcinoma (ccRCC).Epigenetics · 2025Article
- HOTAIR requires epitranscriptomic modification to exert its pivotal epigenetic role in Epithelial to Mesenchymal Transition.Cell death & disease · 2025Article
- Integrating machine learning and protein-ligand interaction profiling for the discovery of METTL3 inhibitors.Scientific reports · 2025Article
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- Rethinking RNA Modifications: Therapeutic Strategies for Targeting Dysregulated RNA.Journal of molecular biology · 2025Review
- Role of m6A RNA methylation regulators in pancreatic cancer: interactions and potential implications.Cancer cell international · 2025Review
- Dynamic modifications of circular RNAs drive oncogenesis.Epigenomics · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
Abstract
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Identifiers
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.