ReviewOncotarget2019
The multifaceted anti-cancer effects of BRAF-inhibitors.
Review in Oncotarget, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
- Molecular profile of FLT3-mutated relapsed/refractory patients with AML in the phase 3 ADMIRAL study of gilteritinib.Blood advances · 2022Trial
- Pathogenic mechanism of extracranial arteriovenous malformations: insights from clinical, pathological, and genetic analyses.Virchows Archiv : an international journal of pathology · 2026Article
- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- Multiomics Analysis Reveals Molecular Changes during Early Progression of Precancerous Lesions to Lung Adenocarcinoma in Never-Smokers.Cancer research · 2025Article
- Advances in Understanding Drug Resistance Mechanisms and Innovative Clinical Treatments for Melanoma.Current treatment options in oncology · 2024Review
- FLT3 targeting in the modern era: from clonal selection to combination therapies.International journal of hematology · 2024Review
- Article
- DNA Sequencing of CD138 Cell Population Reveals TP53 and RAS-MAPK Mutations in Multiple Myeloma at Diagnosis.Cancers · 2024Article
- Characterization of dabrafenib-induced drug insensitivity via cellular barcoding and collateral sensitivity to second-line therapeutics.Scientific reports · 2024Article
- Utilizing CD44v6 and V600EBRAF-mutation for in vitro targeted combination therapy of thyroid carcinomas.Heliyon · 2023Article
- Long term activity of vemurafenib in cancers with BRAF mutations: the ACSE basket study for advanced cancers other than BRAFESMO open · 2023Article
- Microbiota, Oxidative Stress, and Skin Cancer: An Unexpected Triangle.Antioxidants (Basel, Switzerland) · 2023Review
- Recurrent central nervous system Rosai-Dorfman disease with KRAS mutation: a case report.Diagnostic pathology · 2023Article
- Canonical Wnt and TGF-β/BMP signaling enhance melanocyte regeneration but suppress invasiveness, migration, and proliferation of melanoma cells.Frontiers in cell and developmental biology · 2023Article
- Advances in the systemic treatment of therapeutic approaches in biliary tract cancer.ESMO open · 2022Review
- Synthesis and evaluation of new chalcones and oximes as anticancer agents.RSC advances · 2022Article
- Editorial: Further advances in understanding the endocrine cancer microenvironment.Frontiers in endocrinology · 2022Article
- gcMECM: graph clustering of mutual exclusivity of cancer mutations.BMC bioinformatics · 2021Article
- Plasma proteome alterations by MAPK inhibitors in BRAFNeoplasia (New York, N.Y.) · 2021Article
- Upregulation of TRIB2 by Wnt/β-catenin activation in BRAFCancer chemotherapy and pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BRAF gene is commonly involved in normal processes of cell growth and differentiation. The BRAF (V600E) mutation is found in several human cancer, causing an increase of cell proliferation due to a modification of the ERK/MAPK-signal cascade. In particular, BRAFV600E mutation is found in those melanoma or thyroid cancer refractory to the common therapy and with a more aggressive phenotype. BRAF V600E was found to influence the composition of the so-called tumour microenvironment modulating both solid (immune-cell infiltration) and soluble (chemokines) mediators, which balance characterize the ultimate behaviour of the tumour, making it more or less aggressive. In particular, the presence of BRAFV600E mutation would be associated with a change of this balance to a more aggressive phenotype of the tumour and a worse prognosis. The investigation of the possible modulation of those components of tumour microenvironment is nowadays object of several studies as a new potential target therapy in those more complicated cases. At present several clinical trials both in melanoma and thyroid cancer are using BRAF-inhibitors with encouraging results, which are derived also from numerous
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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.