SynthesisMedical oncology (Northwood, London, England)2023
BRAF inhibitors in BRAF V600E-mutated ameloblastoma: systematic review of rare cases in the literature.
Synthesis in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Targetable alterations and personalized treatment in ameloblastoma: results from a prospective observational precision oncology study.NPJ precision oncology · 2026Article
- Oncogenic signaling pathways in ameloblastoma and their implications for precision based therapy.Discover oncology · 2026Review
- Comparative Performance Evaluation of GCN, GAT, and GraphSAGE Architectures for Drug-Gene Interaction Prediction in Ameloblastoma via MEK-Pathway Targeting.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Metastasizing Ameloblastoma Mimicking Squamous Cell Carcinoma of the Lung and Harboring an AKT1 Mutation.Head and neck pathology · 2025Article
- Hybrid chalcone-pyrazoline derivatives: synthesis and in silico evaluation for anticancer potential.Future medicinal chemistry · 2025Article
- Molecular-targeted therapy in ameloblastoma: a systematic review.Archives of craniofacial surgery · 2025Article
- The Effect of Conservative vs. Radical Treatment of Ameloblastoma on Recurrence Rate and Quality of Life: An Umbrella Review.Journal of clinical medicine · 2024Review
- Efficiency of B-RAF-/MEK-inhibitors in B-RAF mutated Ameloblastoma: Case report and review of literature.Heliyon · 2023Article
- Identification of ferroptosis-related proteins in ameloblastoma based on proteomics analysis.Journal of cancer research and clinical oncology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmeloblastoma in 66% of the cases harbor a somatic mutation of the "mitogen-activated protein kinase" signaling pathway (BRAF V600E). In V600E mutations, BRAF is in the permanent "on" state and relays the growth-promoting signals independently of the EGFR pathway. Therefore, mutant BRAF represents a target for handful of new drugs.
methodsWe conducted a literature search, with the search terms "Vemurafenib, Dabrafenib, Ameloblastoma, and BRAF." These included seven case reports with nine patients who underwent monotherapy with Dabrafenib or Vemurafenib or combination therapy with Dabrafenib and Trametinib.
resultsThe patients age ranges from 10 years up to 86 years. The distribution of women and men is 4:5. Patients with an initial diagnosis of ameloblastoma, as well as recurrences or metastasized ameloblastoma were treated. Indications cover neoadjuvant therapy up to the use in metastasized patients in an irresectable state. Results ranging from "only" tumor size reduction to restitutio ad integrum.
conclusionWe see the use of BRAF Inhibitors to reduce tumor size with consecutive surgical treatment as a reasonable option for therapy. However, we are aware that at present the data are based only on case reports with the longest follow-up of just 38 months. We encourage further clinical trials in the use of BRAF Inhibitors for selecting ameloblastoma patients in a multi-center setting.
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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.