ArticleThe Journal of clinical investigation2019
Profound MEK inhibitor response in a cutaneous melanoma harboring a GOLGA4-RAF1 fusion.
Article in The Journal of clinical investigation, 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
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- Gene fusions in melanocytic lesions: an updated comprehensive review.Journal of pathology and translational medicine · 2026Article
- Molecular Landscape of Pediatric Low-Grade Gliomas: Insights From RNA-NGS and Bioinformatic Analysis.Genes, chromosomes & cancer · 2025Article
- Genomic profiling and personalized treatment strategies for skin malignancies: findings from the center for cancer genomics and advanced therapeutics database.International journal of clinical oncology · 2025Review
- Targeting RAF1 gene fusions with MEK inhibition in metastatic melanoma.The oncologist · 2025Article
- Genomic landscape of cutaneous, acral, mucosal, and uveal melanoma in Japan: analysis of clinical comprehensive genomic profiling data.International journal of clinical oncology · 2024Article
- Expanding the landscape of oncogenic drivers and treatment options in acral and mucosal melanomas by targeted genomic profiling.International journal of cancer · 2024Article
- Exploring Molecular Genetic Alterations and RAF Fusions in Melanoma: A Belvarafenib Expanded Access Program in Patients with RAS/RAF-Mutant Melanoma.The oncologist · 2024Article
- The role of CRAF in cancer progression: from molecular mechanisms to precision therapies.Nature reviews. Cancer · 2024Review
- Targeting CRAF kinase in anti-cancer therapy: progress and opportunities.Molecular cancer · 2023Review
- Exceptional Response to MEK Inhibition in a Patient With RAF1-Mutant Myxofibrosarcoma: Case Report and Mechanistic Overview.JCO precision oncology · 2023Article
- Article
- Transcriptional Profiling of Malignant Melanoma Reveals Novel and Potentially Targetable Gene Fusions.Cancers · 2022Article
- Sustained Response to the Mitogen-Activated Extracellular Kinase Inhibitor Trametinib in a Spindle Cell Sarcoma Harboring a QKI-RAF1 Gene Fusion.JCO precision oncology · 2022Article
- Durable Response of Dabrafenib, Trametinib, and Capmatinib in an NSCLC Patient With Co-Existing BRAF-KIAA1549 Fusion and MET Amplification: A Case Report.Frontiers in oncology · 2022Article
- Unearthing novel fusions as therapeutic targets in solid tumors using targeted RNA sequencing.Frontiers in oncology · 2022Article
- RAF1-rearranged spindle cell tumour: report of two additional cases with identification of a novel FMR1-RAF1 fusion.Virchows Archiv : an international journal of pathology · 2021Article
- Accurate and efficient detection of gene fusions from RNA sequencing data.Genome research · 2021Article
- Identification of Tumor Microenvironment-Related Alternative Splicing Events to Predict the Prognosis of Endometrial Cancer.Frontiers in oncology · 2021Article
- Identification of Targetable Gene Fusions and Structural Rearrangements to Foster Precision Medicine inJCO precision oncology · 2021Article
- Targetable BRAF and RAF1 Alterations in Advanced Pediatric Cancers.The oncologist · 2021Article
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRAF and CRAF are critical components of the MAPK signaling pathway which is activated in many cancer types. In approximately 1% of melanomas, BRAF or CRAF are activated through structural arrangements. We describe here a metastatic melanoma with a GOLGA4-RAF1 fusion and pathogenic variants in CTNNB1 and CDKN2A. Anti-CTLA4/anti-PD1 combination immunotherapy failed to control tumor progression. In the absence of other actionable variants the patient was administered MEK inhibitor therapy on the basis of its potential action against RAF1 fusions. This resulted in a profound and clinically significant response. We demonstrated that GOLGA4-RAF1 expression was associated with ERK activation, elevated expression of the RAS/RAF downstream co-effector ETV5, and a high Ki67 index. These findings provide a rationale for the dramatic response to targeted therapy. This study shows that thorough molecular characterization of treatment-resistant cancers can identify therapeutic targets and personalize management, leading to improved patient outcomes.
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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.