ArticleGenes, chromosomes & cancer2022
AGAP3: A novel BRAF fusion partner in pediatric pancreatic-type acinar cell carcinoma.
Article in Genes, chromosomes & cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Salivary gland carcinomas with BRAF fusions - an exceedingly rare and yet poorly characterized group of tumors, with potentially targetable molecular alteration.Virchows Archiv : an international journal of pathology · 2026Article
- Pediatric pancreatic acinar cell carcinoma with a non-canonical BRAF-KMT2C fusion and a classic SND1-BRAF fusion: a case report and literature review.BMC pediatrics · 2025Review
- RareHeliyon · 2024Article
- Paediatric pancreatic acinar cell carcinoma with a novel SEC31A-BRAF fusion gene.Virchows Archiv : an international journal of pathology · 2024Article
- Fusion genes in pancreatic tumors.Trends in cancer · 2024Review
- Tumor-Type Agnostic, Targeted Therapies: BRAF Inhibitors Join the Group.Acta medica academica · 2022Review
- AGAP3: A novel BRAF fusion partner in pediatric pancreatic-type acinar cell carcinoma.Genes, chromosomes & cancer · 2022Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most available molecular data on pancreatic acinar cell carcinoma (PACC) are provided by studies of adult cases. BRAF, RAF1, or RET rearrangements have been described in approximately 30% of cases. To the best of our knowledge, only seven cases with molecular data have been reported in pediatric PACC. We report here the comprehensive study of a pancreatic-type ACC from a 6-year-old patient. We detected an AGAP3::BRAF fusion. This result showing a BRAF rearrangement demonstrates a molecular link between adult and pediatric PACC. Moreover, it identifies AGAP3, a gene located at 7q36.1 that encodes a major component of the N-methyl-d-aspartate (NMDA) receptor signaling complex, as a partner gene of BRAF. The variability of BRAF partners is consistent with a driver role of BRAF alterations in PACC. The identification of such alterations is noteworthy for considering the use of MEK inhibitors in metastatic cases. We did not detect associated genomic instability. The better outcome of pediatric cases might be related to their stable genomic background.
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