ReviewFrontiers in oncology2019
RAS: Striking at the Core of the Oncogenic Circuitry.
Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 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
114 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Angiosarcoma: a systematic review of biomarkers in diagnosis, prognosis, and therapeutic strategies.Frontiers in oncology · 2025Pooled it
- Regulation of Membrane Association and Downstream Effector Interaction of K-Ras by Its Hypervariable Region.Membranes · 2026Article
- Reconstitution of Ras-PI3Kγ membrane communication and feedback using light-induced signaling inputs.Nature communications · 2026Article
- Clinical implications of RAS mutations in AML: prognostic significance is based upon the involved gene and mutation complexity.Blood advances · 2026Article
- Benefits and challenges of adding BKM120 to a BI-3406 plus trametinib combination therapy.BMC cancer · 2026Article
- Review
- COSMIC-Linked Ras Mutations at the Interface Between H-Ras and PI3KγBiochemistry · 2026Article
- COSMIC-Linked Ras Mutations at the Interface Between H-Ras and PI3KγbioRxiv : the preprint server for biology · 2026Article
- Characterization of KRASNature communications · 2026Article
- Integrins in cancer: insights into mechanisms and therapeutic potential.Cell communication and signaling : CCS · 2026Review
- Uev1A counteracts oncogeniceLife · 2026Article
- Pan-cancer analysis reveals differential PERK expression across tumour types and its potential as a therapeutic target.Discover oncology · 2026Article
- Regulation of Phosphatidylinositol Synthesis in Human Primordial Placenta.Biomolecules · 2026Article
- Generation of Human Haematopoietic Model Cell Lines Revealed Distinct Replication Stress Tolerance Between Two OncogenicBiomolecules · 2026Article
- Crossroads of cell fate: miR-34-mediated regulation of apoptosis and autophagy in glioblastoma.Discover oncology · 2025Review
- Silver(I) Complexes Bearing S-Alkyl Thiosalicylic Acid Derivatives: DNA/BSA Binding and Antitumor Activity In Vitro and In Vivo.Pharmaceutics · 2025Article
- Co-expression of bovine leukemia virus and bovine foamy virus-derived miRNAs in naturally infected cattle.Microbiology spectrum · 2025Article
- Novel paradigms in KRAS targeting: Unveiling strategies to combat drug resistance.Chinese medical journal · 2025Review
- CRIF counteracts oncogenic Ras and regulates heterochromatin.Molecular genetics and genomics : MGG · 2025Article
- Exploring LAT-derived miRNAs as regulatory agents of EphrinA3 in glioblastoma multiforme.Biochemistry and biophysics reports · 2025Article
54 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
2 authors.
Funding
Abstract
Cancer is a devastating disease process that touches the lives of millions worldwide. Despite advances in our understanding of the genomic architecture of cancers and the mechanisms that underlie cancer development, a great therapeutic challenge remains. Here, we revisit the birthplace of cancer biology and review how one of the first discovered oncogenes, RAS, drives cancers in new and unexpected ways. As our understanding of oncogenic signaling has evolved, it is clear that RAS signaling is not homogenous, but activates distinct downstream effectors in different cancer types and grades. RAS signaling is tightly controlled through a series of post-transcriptional mechanisms, which are frequently distorted in the context of cancer, and establish key metabolic and immunologic states that support cancer growth, migration, survival, metastasis, and plasticity. While targeting RAS has been fiercely pursued for decades, new strategies have recently emerged with the potential for therapeutic efficacy. Thus, understanding the complexities of RAS biology may translate into improved therapies for patients with RAS-driven cancers.
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.