ReviewCancers2019
Targeting Oncogenic BRAF: Past, Present, and Future.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 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
124 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Reliability of BRAF mutation detection using plasma sample: A systematic review and meta-analysisMedicine · 2021Pooled it
- Trial
- High-resolution measurement of ERK activation state reveals determinants of BRAF regulation and drug sensitivity.bioRxiv : the preprint server for biology · 2026Article
- Targeting MAPK Pathways in Skin, Thyroid, and Pancreatic Cancer: A Perspective on Synthetic Inhibitors and Natural Modulators.Advanced biology · 2026Review
- Beyond EML4: efficacy of targeted therapy in lung cancer patients with rare ALK fusions - a real-world retrospective analysis.NPJ precision oncology · 2026Article
- In silico repurposing of clinically approved drugs as potential BRAF inhibitors: a pharmacophore-based virtual screening and experimental investigation.Cancer cell international · 2026Article
- Natural bioactive molecules and chemotherapeutics synergism for enhanced cancer therapy.Nutrition & metabolism · 2026Review
- Synergistic antitumor effect of oroxylin A and donafenib in hepatocellular carcinoma through tumor protein p53 signaling pathway activation.World journal of gastroenterology · 2026Article
- Pan-RAF inhibitor exarafenib targets BRAF class II/III NSCLC and reveals ARAF-KSR1 resistance and combination strategies.Nature communications · 2026Article
- Single-cell omics in investigating the effect of CAFs with KRAS overexpression on the malignant progression of anaplastic thyroid cancer.Journal of the Chinese Medical Association : JCMA · 2026Article
- Review
- Functionalized nanomedicines for co-targeting of multiple pathways to efficiently treat thyroid cancer: prospects and challenges.Frontiers in pharmacology · 2026Review
- AI-drivenPeerJ · 2026Article
- Targeting BRAF Class II and III Mutations in NSCLC with the pan-RAF inhibitor Exarafenib Reveals ARAF-KSR1-Mediated Resistance and Rational Combination Strategies.Research square · 2025Article
- Article
- Dual targeting of VEGFR2 and CSF1R with SYHA1813 confers novel strategy for treating both BRAF wild-type and mutant melanoma.Cancer cell international · 2025Article
- Cx43 enhances response to BRAF/MEK inhibitors by reducing DNA repair capacity.Nature communications · 2025Article
- High CCR6 expression increases the risk of pediatric Langerhans cell histiocytosis.Blood science (Baltimore, Md.) · 2025Article
- RAS Pathway Mutations and Therapeutics in Vascular Anomalies.Pediatric blood & cancer · 2025Review
- Mutational Landmarks in Anaplastic Thyroid Cancer: A Perspective of a New Treatment Strategy.Journal of clinical medicine · 2025Review
64 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.
Funding
Abstract
Identifying recurrent somatic genetic alterations of, and dependency on, the kinase BRAF has enabled a "precision medicine" paradigm to diagnose and treat BRAF-driven tumors. Although targeted kinase inhibitors against BRAF are effective in a subset of mutant BRAF tumors, resistance to the therapy inevitably emerges. In this review, we discuss BRAF biology, both in wild-type and mutant settings. We discuss the predominant BRAF mutations and we outline therapeutic strategies to block mutant BRAF and cancer growth. We highlight common mechanistic themes that underpin different classes of resistance mechanisms against BRAF-targeted therapies and discuss tumor heterogeneity and co-occurring molecular alterations as a potential source of therapy resistance. We outline promising therapy approaches to overcome these barriers to the long-term control of BRAF-driven tumors and emphasize how an extensive understanding of these themes can offer more pre-emptive, improved therapeutic strategies.
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.