ReviewNPJ precision oncology2022
Molecular pathogenesis of desmoid tumor and the role of γ-secretase inhibition.
Review in NPJ precision oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Pooled it
- Nirogacestat, a γ-Secretase Inhibitor for Desmoid Tumors.The New England journal of medicine · 2023Trial
- Expert opinion document on the management of desmoid tumours in adult patients in Spain.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Axillary desmoid-type fibromatosis: a rare clinical presentation, histopathological correlation, and literature review.BMC surgery · 2026Review
- CTNNB1 Mutational analysis enhances diagnostic precision in β-catenin-negative desmoid fibromatosis: a clinicopathological and molecular study.Virchows Archiv : an international journal of pathology · 2026Article
- Mucosa-associated lymphoid tissue lymphoma with monoclonal T-cell expansion.Virchows Archiv : an international journal of pathology · 2026Article
- UPLC-LCMS-Based Method Development, Validation, Forced Degradation, and Impurity Profiling of Nirogacestat Drug Substance.Current topics in medicinal chemistry · 2026Article
- Asperuloside: an emerging therapeutic candidate for Parkinson's disease through molecular mechanistic insights.Inflammopharmacology · 2025Review
- Matrix stiffness induces endothelial network senescence.bioRxiv : the preprint server for biology · 2025Article
- Pharmacological aspects of FDA-approved novel drug therapies against cancer in 2023: a comprehensive review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Surgical Management of Desmoid Tumors-Patient Selection, Timing, and Approach.Current oncology (Toronto, Ont.) · 2025Review
- Notch signaling in cancers: mechanism and potential therapy.Frontiers in cell and developmental biology · 2025Review
- Case Report: Nirogacestat therapy induces rapid response in a patient with refractory, life-threatening desmoid tumor.Frontiers in oncology · 2025Article
- Efficacy and safety of systemic treatment for progressive and refractory desmoid tumor: a systematic review and Bayesian network meta-analysis.Discover oncology · 2024Article
- Desmoid Tumor after Sleeve Gastrectomy: Case Report and Literature Review.GE Portuguese journal of gastroenterology · 2024Article
- Article
- Nirogacestat: First Approval.Drugs · 2024Review
- Surgical techniques and effectiveness of laparoscopic resection of abdominal wall desmoid-type fibromatosis and defect reconstruction: a single-center retrospective analysis.Hernia : the journal of hernias and abdominal wall surgery · 2024Article
- Capturing Patient Voice to Improve Outcomes That Matter to Patients with Desmoid Tumor.Cancer management and research · 2024Review
- Function of Long Noncoding RNAs in Glioma Progression and Treatment Based on the Wnt/β-Catenin and PI3K/AKT Signaling Pathways.Cellular and molecular neurobiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desmoid tumor (DT) is a rare, soft tissue neoplasm associated with an unpredictable clinical course. Although lacking metastatic potential, DT is often locally aggressive and invasive, causing significant morbidity. Both sporadic DT and familial adenomatous polyposis (FAP)-associated DT are linked to constitutive activation of the Wnt signaling pathway with mutations in the β-catenin oncogene CTNNB1 or the tumor suppressor gene APC, respectively. Cross-talk between the Notch and Wnt pathways, as well as activation of the Notch pathway resulting from dysregulation of the Wnt pathway, suggest a possible therapeutic target for DT. Due to the role γ-secretase plays in Notch signaling through cleavage of the Notch intracellular domain (with subsequent translocation to the nucleus to activate gene transcription), γ-secretase inhibitors (GSIs) have emerged as a potential treatment for DT. Two GSIs, nirogacestat (PF-03084014) and AL102 are in later-stage clinical development; nirogacestat is being evaluated in a phase 3, randomized, placebo-controlled trial while AL102 is being evaluated in a phase 2/3, dose-finding (part A) and placebo-controlled (part B) trial. This review summarizes current understanding of the molecular pathogenesis of DT focusing on dysregulation of the Wnt signaling pathway, crosstalk with the Notch pathway, and the potential therapeutic role for GSIs in DT.
Identifiers
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Registered trials
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.