ArticleNature2022
Silent mutations reveal therapeutic vulnerability in RAS Q61 cancers.
Article in Nature, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 61 citations in OpenAlex.
- KRAS signaling networks, mutational heterogeneity, and emerging therapeutic strategies for cancer treatment.Biomarker research · 2026Review
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.Nature genetics · 2026Article
- Omega Nucleic Acids (ΩNA), Ultimate Nucleic Acids for Future Technology.Molecules (Basel, Switzerland) · 2026Review
- Alternative splicing in cancer drug resistance: Mechanisms and therapeutic prospects (Review).Oncology reports · 2026Review
- Correlation analysis between RAS gene mutations and pathological morphological features in colorectal cancer.Scientific reports · 2025Article
- To be or not to be a protein coding mutation, that's the question!NAR genomics and bioinformatics · 2025Review
- Mutation of CMTR2 in Lung Adenocarcinoma Alters RNA Alternative Splicing and Reveals Therapeutic Vulnerabilities.Nature communications · 2025Article
- Problems in Cancer Genome Medicine: Base Mutations Cause Intron Start Signals, Resulting in Unexpected Splicing.World journal of oncology · 2025Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.bioRxiv : the preprint server for biology · 2025Article
- EZH2 variants derived from cryptic splice sites govern distinct epigenetic patterns during embryonic development.Nucleic acids research · 2025Article
- Review
- Reannotation of cancer mutations based on expressed RNA transcripts reveals functional non-coding mutations in melanoma.American journal of human genetics · 2025Article
- Aquaporin 9 downregulation in KRASScientific reports · 2025Article
- Article
- RNA sensing induced by chromosome missegregation augments anti-tumor immunity.Molecular cell · 2025Article
- Review
- Systematically developing a registry of splice-site creating variants utilizing massive publicly available transcriptome sequence data.Nature communications · 2025Article
- Molecular Basis of Breast Tumor Heterogeneity.Advances in experimental medicine and biology · 2025Review
- Aberrant pre-mRNA processing in cancer.The Journal of experimental medicine · 2024Review
- Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma.NPJ precision oncology · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RAS family members are the most frequently mutated oncogenes in human cancers. Although KRAS(G12C)-specific inhibitors show clinical activity in patients with cancer
Indexed as
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.