ReviewOncogene2011
Raf kinases in cancer-roles and therapeutic opportunities.
Review in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 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
143 citing papers in PubMed, 1 synthesis or guideline pooled it, 293 citations in OpenAlex.
- BRAF inhibitors in BRAF V600E-mutated ameloblastoma: systematic review of rare cases in the literature.Medical oncology (Northwood, London, England) · 2023Pooled it
- Progress on quinoline‑based antitumour agents: Mechanistic insights and optimization strategies (Review).Molecular medicine reports · 2026Review
- A‑Raf: A serine/threonine protein kinase with important biological functions (Review).Molecular medicine reports · 2026Review
- Decoding the Raf-Mek-Erk-Rsk pathway in prostate cancer: from molecular mechanisms to clinical opportunities.British journal of cancer · 2026Review
- Review
- Recent Advances in Benzimidazole-Triazole Hybrids for Single- and Multi-Target Protein Kinase Inhibition.Pharmaceuticals (Basel, Switzerland) · 2026Review
- In silico design of natural-based structures as drug candidates to inhibit ROS1 protein.Scientific reports · 2025Article
- An in vitro BRAF activation assay elucidates molecular mechanisms driving disassembly of the autoinhibited BRAF state.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Profiling with senescence-associated secretory phenotype score identifies GDC-0879 as a small molecule sensitizing glioblastoma to anti-PD1.Cell death & disease · 2025Article
- Impact of Drug-Drug Interactions on Clinical Outcomes in Metastatic Melanoma Patients Treated With Combined BRAF/MEK Inhibitors: A Real-World Study.Pigment cell & melanoma research · 2025Observational
- BRD9 promotes the malignant phenotype of thyroid cancer by activating the MAPK/ERK pathway.Anti-cancer drugs · 2025Article
- PKMYT1 kinase ameliorates cisplatin sensitivity in osteosarcoma.Signal transduction and targeted therapy · 2025Article
- Development and Validation of an Extracellular Matrix Gene Expression Signature for Prognostic Prediction in Patients with Uveal Melanoma.International journal of molecular sciences · 2025Article
- The multifaceted anticancer potential of luteolin: involvement of NF-κB, AMPK/mTOR, PI3K/Akt, MAPK, and Wnt/β-catenin pathways.Inflammopharmacology · 2025Review
- Prognostic markers and molecular pathways in primary colorectal cancer with a high potential of liver metastases: a systems biology approach.Research in pharmaceutical sciences · 2025Article
- Unraveling cutaneous histiocytosis: insights into histology, pathogenesis, diagnosis, and treatment pitfalls.Frontiers in medicine · 2025Review
- An Optimized CRISPR/Cas12a Assay to Facilitate the BRAF V600E Mutation Detection.Journal of clinical laboratory analysis · 2024Article
- Cellular and molecular events in colorectal cancer: biological mechanisms, cell death pathways, drug resistance and signalling network interactions.Discover oncology · 2024Review
- Pyrazolopyridine-based kinase inhibitors for anti-cancer targeted therapy.RSC medicinal chemistry · 2024Review
- ERK pathway agonism for cancer therapy: evidence, insights, and a target discovery framework.NPJ precision oncology · 2024Review
83 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Raf are conserved, ubiquitous serine/protein kinases discovered as the cellular elements hijacked by transforming retroviruses. The three mammalian RAF proteins (A, B and CRAF) can be activated by the human oncogene RAS, downstream from which they exert both kinase-dependent and kinase-independent, tumor-promoting functions. The kinase-dependent functions are mediated chiefly by the MEK/ERK pathway, whose activation is associated with proliferation in a broad range of human tumors. Almost 10 years ago, activating BRAF mutations were discovered in a subset of human tumors, and in the past year treatment with small-molecule RAF inhibitors has yielded unprecedented response rates in melanoma patients. Thus, Raf qualifies as an excellent molecular target for anticancer therapy. This review focuses on the role of BRAF and CRAF in different aspects of carcinogenesis, on the success of molecular therapies targeting Raf and the challenges they present.
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.