Fibromatosis, Aggressive
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Subject Areas on Research
- A Metabolomics Pilot Study on Desmoid Tumors and Novel Drug Candidates.
- A germline mutation at the extreme 3' end of the APC gene results in a severe desmoid phenotype and is associated with overexpression of beta-catenin in the desmoid tumor.
- A high throughput screen identifies Nefopam as targeting cell proliferation in β-catenin driven neoplastic and reactive fibroproliferative disorders.
- Activating mutations of Gs protein in monostotic fibrous lesions of bone.
- Adenomatous polyposis coli gene mutation alters proliferation through its beta-catenin-regulatory function in aggressive fibromatosis (desmoid tumor).
- Aggressive fibromatosis (desmoid tumor) is a monoclonal disorder.
- An association between the 4G polymorphism in the PAI-1 promoter and the development of aggressive fibromatosis (desmoid tumor) in familial adenomatous polyposis patients.
- Biphenotypic sarcoma with characteristics of both a Ewing sarcoma and a desmoplastic small round cell tumor.
- Bone Morphogenetic Proteins Are Expressed by Both Bone-Forming and Non-Bone-Forming Lesions.
- CRISPR-SID: Identifying EZH2 as a druggable target for desmoid tumors via in vivo dependency mapping.
- Combination therapy with sorafenib and celecoxib for pediatric patients with desmoid tumor.
- Commentary: A Novel Method to Treat Progressive Desmoid Tumors Involving Neurovascular Bundles: A Retrospective Cohort Study.
- Cortical desmoid and the four clinical scenarios.
- Cyclooxygenase-two (COX-2) modulates proliferation in aggressive fibromatosis (desmoid tumor).
- Desmoid tumors of the chest wall.
- Efficacy of auranofin as an inhibitor of desmoid progression.
- Estrogen receptor-beta expression in extraabdominal fibromatoses: an analysis of 40 cases.
- Evolving strategies for management of desmoid tumor.
- Familial adenomatous polyposis-associated desmoids display significantly more genetic changes than sporadic desmoids.
- Fibromatoses in childhood: the desmoid/fibromatosis complex.
- Genetic deletion of receptor for hyaluronan-mediated motility (Rhamm) attenuates the formation of aggressive fibromatosis (desmoid tumor).
- Human sterile alpha motif domain 9, a novel gene identified as down-regulated in aggressive fibromatosis, is absent in the mouse.
- IFN-{beta} signaling positively regulates tumorigenesis in aggressive fibromatosis, potentially by modulating mesenchymal progenitors.
- Identical twin small bowel transplant after resection of abdominal desmoid tumor.
- Identical-twin small-bowel transplant for desmoid tumour.
- In desmoid-type fibromatosis cells sorafenib induces ferroptosis and apoptosis, which are enhanced by autophagy inhibition.
- Increased beta-catenin protein and somatic APC mutations in sporadic aggressive fibromatoses (desmoid tumors).
- Intra-abdominal desmoid tumor after successful treatment for Hodgkin disease.
- Intrathoracic desmoid tumor: brief report and review of literature.
- Invasion and MMP expression profile in desmoid tumours.
- Management and recurrence patterns of desmoids tumors: a multi-institutional analysis of 211 patients.
- Marginal versus segmental mandibulectomy for pediatric desmoid fibromatosis of the mandible - Two case reports and review of the literature.
- Molecular genetic and immunohistochemical analysis of the tumor suppressor genes Rb and p53 in palmar and aggressive fibromatosis.
- Nirogacestat, a γ-Secretase Inhibitor for Desmoid Tumors.
- Optimal therapy for desmoid tumors: current options and challenges for the future.
- Plasminogen activator inhibitor-1 (PAI-1) modifies the formation of aggressive fibromatosis (desmoid tumor).
- Platelet-derived growth factor in fibrous musculoskeletal disorders: a study of pathologic tissue sections and in vitro primary cell cultures.
- Sorafenib for Advanced and Refractory Desmoid Tumors.
- Systemic inflammatory response syndrome after human syngeneic intestinal transplantation: evidence for disruption of enterocyte barrier function.
- Targeting stem cell behavior in desmoid tumors (aggressive fibromatosis) by inhibiting hedgehog signaling.
- Tcf-3 expression and beta-catenin mediated transcriptional activation in aggressive fibromatosis (desmoid tumour).
- Testosterone regulates cell proliferation in aggressive fibromatosis (desmoid tumour).
- The management of desmoid tumours: A joint global consensus-based guideline approach for adult and paediatric patients.
- beta-Catenin stabilization dysregulates mesenchymal cell proliferation, motility, and invasiveness and causes aggressive fibromatosis and hyperplastic cutaneous wounds.