ArticleMolecular oncology2017
β-Catenin in desmoid-type fibromatosis: deep insights into the role of T41A and S45F mutations on protein structure and gene expression.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- Management of Desmoid Tumors.Current oncology reports · 2025Review
- Active Surveillance in Patients with Extra-abdominal Desmoid-Type Fibromatosis: A Pooled Analysis of Three Prospective Observational Studies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Observational
- Genomic, Epigenomic, and Transcriptomic Inter- and Intratumor Heterogeneity in Desmoid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Intraabdominal sporadic desmoid tumors and inflammation: an updated literature review and presentation and insights on pathogenesis of synchronous sporadic mesenteric desmoid tumors occurring after surgery for necrotizing pancreatitis.Clinical and experimental medicine · 2023Review
- Clinicopathological assessment of PD-1/PD-L1 immune checkpoint expression in desmoid tumors.European journal of histochemistry : EJH · 2023Article
- Article
- Molecular rationale for SARS-CoV-2 spike circulating mutations able to escape bamlanivimab and etesevimab monoclonal antibodies.Scientific reports · 2021Article
- Article
- Development, Validation, and Visualization of A Web-Based Nomogram for Predicting the Recurrence-Free Survival Rate of Patients With Desmoid Tumors.Frontiers in oncology · 2021Article
- Article
- Computational Alanine Scanning and Structural Analysis of the SARS-CoV-2 Spike Protein/Angiotensin-Converting Enzyme 2 Complex.ACS nano · 2020Article
- Clinical benefit of methotrexate plus vinorelbine chemotherapy for desmoid fibromatosis (DF) and correlation of treatment response with MRI.Cancer medicine · 2019Article
- Mutation Hotspots in the β-Catenin Gene: Lessons from the Human Cancer Genome Databases.Molecules and cells · 2019Review
- Locally Aggressive Connective Tissue Tumors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desmoid-type fibromatosis (DF) is a rare mesenchymal lesion with high risk of local recurrence. Specific β-catenin mutations (S45F) appeared to be related to this higher risk compared to T41A-mutated or wild-type (WT). We explored the influence of both mutations and WT on structure stability and affinity of β-catenin for α-catenin and the pattern of gene expression that may influence DF behavior. Using 33 surgically resected primary DFs harboring T41A (n = 14), S45F (n = 10), or WT (n = 9), we performed a comparative molecular analysis by protein/protein interaction modeling, gene expression by DASL microarrays, human inflammation gene panel, and assessment of immune system-based biomarkers by immunohistochemistry. Mutated proteins were more stable than WT and formed a weaker complex with α-catenin. Consensus unsupervised gene clustering revealed the presence of two DF group-mutated (T41A + S45F) and WT (P = 0.0047). The gene sets 'Inflammatory-Defense-Humoral Immune Response' and 'Antigen Binding' were significantly enriched in T41A. The deregulation of 16 inflammation-related genes was confirmed. Low numbers of T cells and tumor-associated macrophages (TAM) infiltrating the tumors and low/absent PD-1/PD-L1 expression were also identified. We demonstrated that mutated DFs (T41A or S45F) and WT are two distinct molecular subgroups with regard to β-catenin stability, α-catenin affinity, and gene expression profiling. A different inflammation signature characterized the two mutated groups, suggesting mediation either by T41A or by S45F. Finally, all mutated cases showed a low number of TIL and TAM cells and a low or absent expression of PD-1 and PD-L1 consistent with β-catenin activation insensitive to checkpoint blockade.
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