ArticleThe American journal of pathology1997
Increased beta-catenin protein and somatic APC mutations in sporadic aggressive fibromatoses (desmoid tumors).
Article in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 328 citations in OpenAlex.
- Sorafenib for Advanced and Refractory Desmoid Tumors.The New England journal of medicine · 2018Trial
- 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
- Safety and efficacy of high-dose tamoxifen and sulindac for desmoid tumor in children: results of a Children's Oncology Group (COG) phase II study.Pediatric blood & cancer · 2013Trial
- Intra-Abdominal Sporadic Desmoid Tumors with CanonicalInternational journal of molecular sciences · 2026Article
- Locally Aggressive Desmoid Tumor With L4-L5 Vertebral Invasion and Progressive Neurological Deficit: A Case Report.Clinical case reports · 2026Article
- Desmoid tumor mimicking cancer recurrence in a patient with colon cancer and Gardner syndrome: A case report.SAGE open medical case reports · 2026Article
- Multifocal Desmoid-Type Fibromatosis: Case Series and Potential Relationship to Neuronal Spread.Cureus · 2024Article
- PDGFRβ Signaling Cooperates with β-Catenin to Modulate c-Abl and Biologic Behavior of Desmoid-Type Fibromatosis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- CD142 Identifies Neoplastic Desmoid Tumor Cells, Uncovering Interactions Between Neoplastic and Stromal Cells That Drive Proliferation.Cancer research communications · 2023Article
- Article
- Recurrent CTNNB1 mutations in craniofacial osteomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- CRISPR-SID: Identifying EZH2 as a druggable target for desmoid tumors via in vivo dependency mapping.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Sporadic intra-abdominal desmoid tumor with a very unusual onset: two case reports.Journal of medical case reports · 2021Article
- Percutaneous cryoablation for advanced and refractory extra-abdominal desmoid tumors.International journal of clinical oncology · 2021Article
- Frequent CTNNB1 p.S45 Mutations and Aggressive Clinical Behavior in Neuromuscular Choristoma-Associated Fibromatosis.Neurosurgery · 2021Article
- Ball in the Wall: Mesenteric Fibromatosis-a Rare Case Report.Indian journal of surgical oncology · 2020Article
- Targeted therapy of desmoid-type fibromatosis: mechanism, current situation, and future prospects.Frontiers of medicine · 2019Review
- Article
- Beta-Catenin Mutation with Complex Chromosomal Changes in Desmoid Tumor of the Scalp: A Case Report.Craniomaxillofacial trauma & reconstruction · 2019Article
- Nuclear TFE3 expression is a diagnostic marker for Desmoid-type fibromatosis.Diagnostic pathology · 2019Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic aggressive fibromatosis (also called desmoid tumor) is a monoclonal proliferation of spindle (fibrocyte-like) cells that is locally invasive but does not metastasize. A similarity to abdominal fibromatoses (desmoids) in familial adenomatous polyposis and a cytogenetic study showing partial deletion of 5q in a subset of aggressive fibromatoses suggests that the adenomatous polyposis coli (APC) gene plays a role in its pathogenesis. APC helps regulate the cellular level of beta-catenin, which is a downstream mediator in Wnt (Wingless) signaling. beta-Catenin has a nuclear function (binds transcription factors) and a cell membrane function (is a component of epithelial cell adherens junctions). Six cases of aggressive fibromatosis of the extremities from patients without familial adenomatous polyposis, or a family history of colon cancer, were studied. Immunohistochemistry, using carboxy and amino terminus antibodies to APC, and DNA sequencing showed that three of the six contained an APC-truncating mutation, whereas normal tissues did not contain a mutation. Western blot and Northern dot blot showed that all six tumors had a higher level of beta-catenin protein than surrounding normal tissues, despite containing similar levels of beta-catenin mRNA. Immunohistochemistry localized beta-catenin throughout the cell in tumor tissues, although it localized more to the periphery in cells from normal tissues. Reverse transcription polymerase chain reaction showed that the tumors expressed N-cadherin but not E-cadherin (a pattern of expression of proteins making up adherens junctions similar to fibrocytes), suggesting that the specific adherens junctions present in epithelial cells are not necessary for beta-catenin function. Increased beta-catenin may cause the growth advantage of cells in this tumor through a nuclear mechanism. The increased protein level, relative to the RNA level, suggests that beta-catenin is degraded at a lower rate compared with normal tissues. In some cases, this is caused by a somatic mutation resulting in a truncated APC protein.
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Identifiers
9250146PMC1857985W1854996193What 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.