ReviewOncogene2008
BRAF(E600) in benign and malignant human tumours.
Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 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
122 citing papers in PubMed, 269 citations in OpenAlex.
- Phase II Pilot Study of Vemurafenib in Patients With Metastatic BRAF-Mutated Colorectal Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015Trial
- Nucleoporin TPR integrates MAPK signaling with mitogen-induced transcriptional programs.Cell death & disease · 2026Article
- Diffuse low-grade glioma with a rare BRAF p.T599dup mutation in a child: importance of clinicopathological and molecular correlation.Brain tumor pathology · 2026Article
- Oral and Craniofacial Development and Immunology.Advances in experimental medicine and biology · 2026Review
- BRAF mutations and targeted therapy in unclassified pericytic tumors: insights from genetic analysis and clinical response.BMC cancer · 2025Article
- A multi-center cross-sectional investigation ofPeerJ · 2025Article
- Prediction and Validation of Novel BRAF Inhibitor as a Potential Drug Candidate for the Treatment of Colorectal Cancer.Current topics in medicinal chemistry · 2025Article
- Update on Neoadjuvant and Adjuvant BRAF Inhibitors in Papillary Craniopharyngioma: A Systematic Review.Cancers · 2024Review
- Frequency of BRAF Mutations in Dysplastic Nevi, Lentigo Maligna, and Melanoma In Situ.Journal of clinical medicine · 2024Article
- DNA Sequencing of CD138 Cell Population Reveals TP53 and RAS-MAPK Mutations in Multiple Myeloma at Diagnosis.Cancers · 2024Article
- Spatial resolution of cellular senescence dynamics in human colorectal liver metastasis.Aging cell · 2023Article
- Multi-range ERK responses shape the proliferative trajectory of single cells following oncogene induction.Cell reports · 2023Article
- Current Advances in Papillary Craniopharyngioma: State-Of-The-Art Therapies and Overview of the Literature.Brain sciences · 2023Review
- Recent and Future Strategies to Overcome Resistance to Targeted Therapies and Immunotherapies in Metastatic Colorectal Cancer.Journal of clinical medicine · 2022Review
- Review
- Multigene Panel Sequencing Reveals Cancer-Specific and Common Somatic Mutations in Colorectal Cancer Patients: An Egyptian Experience.Current issues in molecular biology · 2022Article
- Review
- Review
- Review
- Precise Characterization of Genetic Interactions in Cancer via Molecular Network Refining Processes.International journal of molecular sciences · 2021Article
62 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
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Of the RAF family of protein kinases, BRAF is the only member to be frequently activated by mutation in cancer. A single amino acid substitution (V600E) accounts for the vast majority and results in constitutive activation of BRAF kinase function. Its expression is required to maintain the proliferative and oncogenic characteristics of BRAF(E600)-expressing human tumour cells. Although BRAF(E600) acts as an oncogene in the context of additional genetic lesions, in primary cells it appears to be associated rather with transient stimulation of proliferation. Eventually, BRAF(E600) signalling triggers cell cycle arrest with the hallmarks of cellular senescence, as is illustrated by several recent studies in cultured cells, animal models and benign human lesions. In this review, we will discuss recent advances in our understanding of the role of BRAF(E600) in benign and malignant human tumours and the implications for therapeutic intervention.
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.