ArticleNature communications2025
Wnt/β-catenin activation by mutually exclusive FBXW11 and CTNNB1 hotspot mutations drives salivary basal cell adenoma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Integrating Histological and Molecular Findings for Practical Salivary Gland Diagnostics.Head and neck pathology · 2026Review
- Imaging of benign salivary gland tumors under the fifth WHO classification, with a focus on rare histologic types and newly listed entities-Part II.Japanese journal of radiology · 2026Review
- Transcription factor targeting strategies in cancer: mechanisms, challenges and cutting-edge progress.Acta pharmacologica Sinica · 2026Review
- Insights From Mutational and Transcriptomic Profiles in Epithelial-myoepithelial Carcinoma.The American journal of surgical pathology · 2026Article
- CircSPARC promotes esophageal squamous cell carcinoma through an HNRNPC-EPN2 splicing axis that activates Wnt/β-Catenin signaling.Molecular cancer · 2026Article
- Mutational scanning reveals oncogenic CTNNB1 mutations have diverse effects on signaling.Nature genetics · 2026Article
- Whole-Exome Profiling of Epstein-Barr Virus-Positive Neuroendocrine Carcinoma of the Nasopharynx.Endocrine pathology · 2026Article
- APC-related multiple salivary gland lesions: spatial transcriptomic analysis reveals progressive WNT activation.The Journal of pathology · 2025Article
- SPARKI: a tool for the statistical analysis of pathogen identification results.Bioinformatics (Oxford, England) · 2025Article
- Integrative diagnostic approach to salivary gland tumors: from clinical evaluation to molecularly targeted therapy.Virchows Archiv : an international journal of pathology · 2025Review
Corrections and comments
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Authors and funding
28 authors.
Funding
Abstract
Basal cell adenoma (BCA) and basal cell adenocarcinoma (BCAC) of the salivary gland are rare tumours that can be difficult to distinguish from each other and other salivary gland tumour subtypes. Using next-generation sequencing, we identify a recurrent FBXW11 missense mutation (p.F517S) in BCA that is mutually exclusive with the previously reported CTNNB1 p.I35T gain-of-function (GoF) mutation with these mutations collectively accounting for 94% of BCAs. In vitro, mutant FBXW11 is characterised by defective binding to β-catenin and higher protein levels within the nucleus. This is consistent with the increased nuclear expression of β-catenin and activation of the Wnt/β-catenin pathway. The genomic profiles of BCAC are distinct from BCA, with hotspot DICER1 and HRAS mutations and putative driver mutations affecting PI3K/AKT and NF-κB signalling pathway genes. These findings have important implications for the diagnosis and treatment of BCA and BCAC, which, despite histopathologic overlap, may be unrelated entities.
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