ArticleCancer2015
Targeting the Notch pathway: A potential therapeutic approach for desmoid tumors.
Article in Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
44 citing papers in PubMed, 80 citations in OpenAlex.
- Nirogacestat, a γ-Secretase Inhibitor for Desmoid Tumors.The New England journal of medicine · 2023Trial
- Whole-Genome and Transcriptome Sequencing Identified NOTCH2 and HES1 as Potential Markers of Response to Imatinib in Desmoid Tumor (Aggressive Fibromatosis): A Phase II Trial Study.Cancer research and treatment · 2022Trial
- Clinical Activity of the γ-Secretase Inhibitor PF-03084014 in Adults With Desmoid Tumors (Aggressive Fibromatosis).Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2017Trial
- Molecular Mechanisms Underlying Progression and Spontaneous Regression in Desmoid Tumors.International journal of molecular sciences · 2026Review
- Review
- Systemic Therapies for Desmoid Tumors: A Review of Past, Present, and Future Treatments.Cancers · 2026Review
- Glycemic variability associated with gamma secretase inhibitor therapy in a type 1 diabetic patient undergoing treatment for desmoid tumor: a case report.Frontiers in endocrinology · 2026Article
- Review
- Repurposing nirogacestat, a gamma secretase enzyme inhibitor in desmoid tumors.Future oncology (London, England) · 2025Review
- Single-Cell Transcription Reveals the Fibroblast Heterogeneity and Neural Cells' Significance in Desmoid Fibromatosis.Cancer science · 2025Article
- 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
- Fibromatosis of the accessory breast mimicking a malignant tumor: a rare case report and literature review.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
- Management of Desmoid Disease in Familial Adenomatous Polyposis.Clinics in colon and rectal surgery · 2024Review
- Nirogacestat: First Approval.Drugs · 2024Review
- Desmoid Tumors: Current Perspective and Treatment.Current treatment options in oncology · 2024Review
- Current Treatment Concepts for Extra-Abdominal Desmoid-Type Fibromatosis: A Narrative Review.Cancers · 2024Review
- Desmoid Tumors: A Comprehensive Review.Advances in therapy · 2023Review
- Targeted therapies for the treatment of soft tissue sarcoma.Frontiers in oncology · 2023Review
- Clinical Prognostic Factors and Integrated Multi-Omics Studies Identify Potential Novel Therapeutic Targets for Pediatric Desmoid Tumor.Biological procedures online · 2022Article
Corrections and comments
- Commented on by
Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundDesmoid tumors (DTs) are rare mesenchymal lesions that can recur repeatedly. When it is feasible, DTs are surgically resected; however, this often results in high recurrence rates. Recently, treatment with PF-03084014, a potent γ-secretase inhibitor, has been shown to have antitumor activity in several tumor types by affecting the WNT/β-catenin pathway. Consequently, Notch pathway inhibition by PF-03084014 might be a promising approach for DT treatment.
methodsThe expression of Notch pathway components was analyzed in DT tissues and cell strains with immunohistochemistry and Western blotting, respectively. A panel of DT cell strains was exposed to PF-03084014 and evaluated for cell proliferation. Antitumor effects were assessed via cell cycle, apoptosis, and migration and invasion analysis. Cells treated with PF-03084014 were characterized with a gene array analysis combined with Ingenuity Pathway Analysis.
resultsThe results showed that Notch pathway components were expressed at different levels in DTs. Hes1 (Hes Family BHLH Transcription Factor 1) was overexpressed in DT tumors versus dermal scar tissue, and PF-03084014 caused significant decreases in Notch intracellular domain and Hes1 expression in DT cell strains. PF-03084014 decreased DT cell migration and invasion and also caused cell growth inhibition in DT cell strains, most likely through cell cycle arrest. Gene array analysis combined with Ingenuity Pathway Analysis showed that Wnt1-inducible signaling pathway protein 2 possibly regulated Notch and WNT pathways after treatment with PF-03084014 through integrin.
conclusionOur findings suggest that the Notch pathway is an important DT therapeutic target. Furthermore, PF-03084014 has significant antitumor activity against DTs, and it may be an alternative strategy for DT treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.