ArticleCancer research2012
Mesenchymal stromal cell mutations and wound healing contribute to the etiology of desmoid tumors.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Does ileoanal pouch surgery increase the risk of desmoid in patients with familial adenomatous polyposis?International journal of colorectal disease · 2020Pooled it
- Phase II clinical trial of nirogacestat in patients with relapsed ovarian granulosa cell tumours.Clinical and translational medicine · 2026Trial
- 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
- Differential [European journal of nuclear medicine and molecular imaging · 2026Article
- Chronic multifocal collagenous fibroma with tumor development at surgical incision site: a 46-year case report.Discover oncology · 2026Article
- Mechanisms and therapeutic potential of the hedgehog signaling pathway in cancer.Cell death discovery · 2025Review
- Molecular characteristics and cancer immunity of LRP1B and its relationship with the Hedgehog signaling pathway in colorectal cancer.Frontiers in immunology · 2025Article
- Case Report: A case of new-onset retroperitoneal aggressive fibromatosis after resection of solid pseudopapillary tumor of the pancreas and review of the literature.Frontiers in oncology · 2025Article
- Article
- 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
- Novel insights into biomarkers of progression in Desmoid tumor.Frontiers in oncology · 2023Review
- Molecular pathogenesis of desmoid tumor and the role of γ-secretase inhibition.NPJ precision oncology · 2022Review
- Article
- Wnt-Independent and Wnt-Dependent Effects of APC Loss on the Chemotherapeutic Response.International journal of molecular sciences · 2020Review
- Article
- [Long-term effectiveness of "West China Classification" guided surgical treatment of desmoid-type fibromatosis in shoulder girdle].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2020Article
- Article
- Activated Signaling Pathways and Targeted Therapies in Desmoid-Type Fibromatosis: A Literature Review.Frontiers in oncology · 2019Review
- Clinical prognostic factors for pediatric extra-abdominal desmoid tumor: analyses of 66 patients at a single institution.World journal of surgical oncology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Desmoid tumors are nonmalignant neoplasms of mesenchymal origin that mainly contain fibroblast lineage cells. These tumors often occur in patients with familial adenomatous polyposis (FAP) coli who have germ line mutations in the APC gene. Given emerging data that has implicated multipotent mesencyhmal stromal cells (MSC) in the origin of mesenchymal tumors, we hypothesized that desmoid tumors may arise in patients with FAP after MSCs acquire somatic mutations during the proliferative phase of wound healing. To test this idea, we examined 16 desmoid tumors from FAP-associated and sporadic cases, finding that all 16 of 16 tumors expressed stem cell markers, whereas matching normal stromal tissues were uniformly negative. Desmoid tumors also contained a subclass of fibrocytes linked to wound healing, angiogenesis, and fibrosis. Using an MSC cell line derived from an FAP-associated desmoid tumor, we confirmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional repressor BMI-1 while documenting the coexpression of markers for chondrocytes, adipocytes, and osteocytes. Together, our findings argue that desmoid tumors result from the growth of MSCs in a wound healing setting that is associated with deregulated Wnt signaling due to APC loss. The differentiation potential of these MSCs combined with expression of BMI-1, a transcriptional repressor downstream of Hedgehog and Notch signaling, suggests that desmoid tumors may respond to therapies targeting these pathways.
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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.