ReviewOncotarget2010
The BRAFV600E mutation: what is it really orchestrating in thyroid cancer?
Review in Oncotarget, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 47 citations in OpenAlex.
- Review
- Nomogram model based on ultrasonography and contrast-enhanced CT for predicting BRAFFrontiers in endocrinology · 2025Article
- Value of a BRAFFrontiers in endocrinology · 2025Article
- Molecular Mutations and Clinical Behavior in Bethesda III and IV Thyroid Nodules: A Comparative Study.Cancers · 2024Article
- Case reports of collision and composite carcinomas of the thyroid: an insight into their origin and clinical significance.BMC endocrine disorders · 2023Article
- Using BioPAX-Parser (BiP) to enrich lists of genes or proteins with pathway data.BMC bioinformatics · 2021Article
- Role of Advanced Glycation End-Products and Other Ligands for AGE Receptors in Thyroid Cancer Progression.Journal of clinical medicine · 2021Review
- Bortezomib sensitizes thyroid cancer to BRAF inhibitorEndocrine-related cancer · 2018Article
- NADPH Oxidase NOX4 Is a Critical Mediator of BRAFAntioxidants & redox signaling · 2017Article
- Article
- Transcriptional and post-translational modifications of B-Raf in quinol-thioether induced tuberous sclerosis renal cell carcinoma.Molecular carcinogenesis · 2016Article
- Genome-wide analysis of differentially expressed miRNA in PLX4720-resistant and parental human thyroid cancer cell lines.Surgery · 2016Article
- Targeted Therapy for MAPK Alterations in Pediatric Gliomas.Brain disorders & therapy · 2015Article
- Article
- Blocks to thyroid cancer cell apoptosis can be overcome by inhibition of the MAPK and PI3K/AKT pathways.Cell death & disease · 2014Article
- Selective anti-cancer agents as anti-aging drugs.Cancer biology & therapy · 2013Article
- Mitochondrial oxidative stress is the Achille's heel of melanoma cells resistant to Braf-mutant inhibitor.Oncotarget · 2013Article
- The prognostic relevance of psammoma bodies and ultrasonographic intratumoral calcifications in papillary thyroid carcinoma.World journal of surgery · 2013Article
- Genotype-dependent cooperation of ionizing radiation with BRAF inhibition in BRAF V600E-mutated carcinomas.Investigational new drugs · 2013Article
- Advances in targeting signal transduction pathways.Oncotarget · 2012Review
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
Abstract
BRAFV600E is a constitutively active onco-kinase and is the most common genetic alteration in papillary thyroid carcinoma (PTC), and in anaplastic thyroid carcinoma as well, albeit at a lower frequency. The BRAFV600E mutation in some studies has been significantly associated with extra-thyroidal extension, metastases, recurrence, and mortality in patients with PTC. A recent genome-wide expression profiling approach (Gene Set Enrichment Analysis (GSEA)) and in vitro and in vivo functional studies revealed that BRAFV600E affects extracellular matrix composition (i.e. increased expression of some collagens and laminins) and promotes thyroid cancer migration and invasion. BRAFV600E through the phospho-MEK1/2 and phospho-ERK1/2 pathway may control a network of genes crucial in integrating and regulating the extracellular and intracellular signaling in thyroid cancer cells, which may be fundamental to trigger an abnormal cell differentiation/totipotency and shape/polarity, and contribute to tumor aggressiveness mechanisms (i.e. cell adhesion, migration, and invasion). Increasing our knowledge of BRAFV600E-modulated ECM genes and targeting the subset of genes essential for tumor aggressiveness will help establish a novel paradigm for treatment of thyroid cancers harboring BRAFV600E. Furthermore, identifying downstream events from the BRAFV600E/ERK1/2 pathway will eventually identify novel biomarkers that can be used to correlate with disease outcome and overall survival.
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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.