Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Introduction to Fibroblasts01:09

Introduction to Fibroblasts

3.9K
Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
3.9K
Fibril-associated Collagen01:11

Fibril-associated Collagen

2.7K
Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
2.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinical Outcomes and Prognostication of CRTC1::TRIM11 Fusion Cutaneous Tumors.

The American journal of surgical pathology·2026
Same author

Subcutaneous para-umbilical low-grade sarcoma with rare FUS::NFATC4 fusion.

Pathology·2026
Same author

Novel perineurioma-like soft tissue tumour with SETD1A::FOSB fusion.

Pathology·2026
Same author

Genomic Landscape of Myoepithelial Carcinoma Tumors.

Oral diseases·2026
Same author

Pleomorphic rhabdomyosarcoma, outcomes of patients with advanced disease treated with systemic agents: Retrospective study from the global pushing ultra-rare sarcomas towards hope (PUSH) consortium.

European journal of cancer (Oxford, England : 1990)·2026
Same author

Novel FGL2::PDGFD and TGFBI::PDGFB Fusions Expand the Molecular Spectrum of Dermatofibrosarcoma Protuberans.

Genes, chromosomes & cancer·2026
Same journal

Impact of the 2025 Endocrine Society clinical practice guideline on the diagnosis and management of primary aldosteronism for the clinical laboratory.

Pathology·2026
Same journal

Cribriform intraductal carcinoma of the prostate may have a greater prognostic impact even than Gleason grade 5 conventional prostatic adenocarcinoma.

Pathology·2026
Same journal

Bordetella pertussis: emerging epidemiology, diagnosis and management.

Pathology·2026
Same journal

Development and validation of a real-time polymerase chain reaction for the detection of Haycocknema perplexum.

Pathology·2026
Same journal

Recent advances in the understanding of TP53 in haematological malignancies.

Pathology·2026
Same journal

Concurrent renal amyloid light chain amyloidosis, light chain crystalline podocytopathy and light chain proximal tubulopathy: a case report.

Pathology·2026
See all related articles

Related Experiment Video

Updated: May 4, 2026

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors
08:57

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors

Published on: May 17, 2024

3.1K

Aggressive fibromatosis.

Cyril Fisher1, Khin Thway

  • 1Royal Marsden Hospital, London, United Kingdom.

Pathology
|January 1, 2014
PubMed
Summary
This summary is machine-generated.

Aggressive fibromatoses are locally invasive tumors that can recur but do not metastasize. Management involves surgery, observation, or therapies like chemotherapy, targeting specific genetic mutations (CTNNB1, APC).

More Related Videos

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

4.5K
An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas
03:53

An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas

Published on: October 10, 2025

679

Related Experiment Videos

Last Updated: May 4, 2026

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors
08:57

Author Spotlight: Genetically Engineered Mouse Models and Pathological Characterization of Neurofibromatosis Type 1 Associated Tumors

Published on: May 17, 2024

3.1K
A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

4.5K
An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas
03:53

An Orthotopic Sciatic Nerve Xenograft for Neurofibromatosis Type 1 Neurofibromas

Published on: October 10, 2025

679

Area of Science:

  • Oncology
  • Genetics
  • Surgical Pathology

Background:

  • Aggressive fibromatoses, also known as desmoid-type fibromatoses, are locally infiltrative collagen-forming tumors.
  • These tumors have a high recurrence rate but do not metastasize, with clinical impact determined by location and biological behavior.
  • Genetic mutations in CTNNB1 (sporadic cases) or APC (familial adenomatous polyposis) are key molecular drivers.

Purpose of the Study:

  • To provide a comprehensive overview of aggressive fibromatoses, including their genetic basis, differential diagnosis, and management strategies.
  • To highlight the importance of clinicopathological subgroups in guiding therapeutic decisions.

Main Methods:

  • Review of existing literature on aggressive fibromatoses.
  • Analysis of genetic mutations (CTNNB1, APC) associated with the condition.
  • Discussion of diagnostic criteria and differential diagnoses.
  • Evaluation of various therapeutic modalities.

Main Results:

  • Aggressive fibromatoses are characterized by local infiltration and recurrence, with no metastatic potential.
  • Somatic CTNNB1 mutations are found in sporadic cases, while germline APC mutations are associated with familial adenomatous polyposis.
  • Differential diagnosis includes other soft tissue tumors, necessitating careful pathological evaluation.
  • Management is primarily surgical, with observation or other therapies (irradiation, hormonal therapy, chemotherapy, tyrosine kinase inhibitors) used for stabilization or tumor shrinkage.

Conclusions:

  • Aggressive fibromatoses require a multidisciplinary approach for optimal management.
  • Tailoring therapy based on genetic profiles and clinicopathological features is crucial for improving outcomes.
  • While surgery is primary, diverse treatment options exist for managing tumor growth and recurrence.