ReviewCancers2019
Epigenetic Mechanisms of Escape from BRAF Oncogene Dependency.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Proteomic Signatures of Vemurafenib Resistance in Canine Urothelial Carcinoma Harboring the BRAFV595E Mutation.Journal of proteome research · 2026Article
- Systematic multivariate analysis of chromatin complex dependencies reveals Set1C/COMPASS as a melanoma-enriched epigenetic vulnerability.PLoS computational biology · 2026Article
- Systematic multivariate analysis of chromatin complex dependencies reveals Set1C/COMPASS as a melanoma-enriched epigenetic vulnerability.bioRxiv : the preprint server for biology · 2026Article
- ABCB5: A Key Regulator Linking Stem Cell Plasticity, Tumor Microenvironment, and Therapy Resistance in Cutaneous Melanoma.Cancers · 2026Review
- Molecular Basis of BRAF Inhibitor Resistance in Melanoma: A Systematic Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Imaging Clusters of Pediatric Low-Grade Glioma Are Associated with Distinct Molecular Characteristics.AJNR. American journal of neuroradiology · 2025Article
- Epigenetic targeting of MECOM/KRAS axis by JIB-04 impairs tumorigenesis and cisplatin resistance in MECOM-amplified ovarian cancer.Cell death discovery · 2025Article
- Mechanism of active component β-sitosterol from Myristica fragrans inducing apoptosis in bladder cancer cells via regulating the BCL-2/BAX/caspase-3 pathway.Frontiers in oncology · 2025Article
- BRAF - a tumour-agnostic drug target with lineage-specific dependencies.Nature reviews. Clinical oncology · 2024Review
- RhoA activation promotes glucose uptake to elevate proliferation in MAPK inhibitor resistant melanoma cells.bioRxiv : the preprint server for biology · 2024Article
- Transcription factor network dynamics during the commitment to oncogene-induced senescence.Frontiers in epigenetics and epigenomics · 2024Article
- Tumor Cell Resistance to the Inhibition of BRAF and MEK1/2.International journal of molecular sciences · 2023Review
- BRAF Mutations in Melanoma: Biological Aspects, Therapeutic Implications, and Circulating Biomarkers.Cancers · 2023Review
- Tumor-Type Agnostic, Targeted Therapies: BRAF Inhibitors Join the Group.Acta medica academica · 2022Review
- NAD/NAMPT and mTOR Pathways in Melanoma: Drivers of Drug Resistance and Prospective Therapeutic Targets.International journal of molecular sciences · 2022Review
- Article
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Interrogating Epigenome toward Personalized Approach in Cutaneous Melanoma.Journal of personalized medicine · 2021Review
- Review
- Many Distinct Ways Lead to Drug Resistance inLife (Basel, Switzerland) · 2021Review
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
About eight percent of all human tumors (including 50% of melanomas) carry gain-of-function mutations in the BRAF oncogene. Mutated BRAF and subsequent hyperactivation of the MAPK signaling pathway has motivated the use of MAPK-targeted therapies for these tumors. Despite great promise, however, MAPK-targeted therapies in BRAF-mutant tumors are limited by the emergence of drug resistance. Mechanisms of resistance include genetic, non-genetic and epigenetic alterations. Epigenetic plasticity, often modulated by histone-modifying enzymes and gene regulation, can influence a tumor cell's BRAF dependency and therefore, response to therapy. In this review, focusing primarily on class 1 BRAF-mutant cells, we will highlight recent work on the contribution of epigenetic mechanisms to inter- and intratumor cell heterogeneity in MAPK-targeted therapy response.
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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.