ArticleThe American journal of pathology2013
Loss of β-catenin induces multifocal periosteal chondroma-like masses in mice.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Molecular, phenotypic aspects and therapeutic horizons of rare genetic bone disorders.BioMed research international · 2014Pooled it
- SAG therapy restores bone growth and reduces enchondroma incidence in a model of skeletal chondrodysplasias caused by Ihh deficiency.Molecular therapy. Methods & clinical development · 2021Article
- Osteochondroma Pathogenesis: Mouse Models and Mechanistic Insights into Interactions with Retinoid Signaling.The American journal of pathology · 2021Review
- Review
- Characterization of Krt19Journal of cellular physiology · 2020Article
- Mechanisms of synovial joint and articular cartilage development.Cellular and molecular life sciences : CMLS · 2019Review
- Possible Contribution of Wnt-Responsive Chondroprogenitors to the Postnatal Murine Growth Plate.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Wnt signaling in cartilage development and diseases: lessons from animal studies.Laboratory investigation; a journal of technical methods and pathology · 2016Review
- Article
- Col2CreER(T2), a mouse model for a chondrocyte-specific and inducible gene deletion.European cells & materials · 2014Review
- Wnt/β-catenin pathway in bone cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Review
- Distribution of slow-cycling cells in epiphyseal cartilage and requirement of β-catenin signaling for their maintenance in growth plate.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2014Article
- Article
- Heparan sulfate in skeletal development, growth, and pathology: the case of hereditary multiple exostoses.Developmental dynamics : an official publication of the American Association of Anatomists · 2013Review
Corrections and comments
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Authors and funding
21 authors at 9 institutions in 3 countries.
Funding
Abstract
Osteochondromas and enchondromas are the most common tumors affecting the skeleton. Osteochondromas can occur as multiple lesions, such as those in patients with hereditary multiple exostoses. Unexpectedly, while studying the role of β-catenin in cartilage development, we found that its conditional deletion induces ectopic chondroma-like cartilage formation in mice. Postnatal ablation of β-catenin in cartilage induced lateral outgrowth of the growth plate within 2 weeks after ablation. The chondroma-like masses were present in the flanking periosteum by 5 weeks and persisted for more than 6 months after β-catenin ablation. These long-lasting ectopic masses rarely contained apoptotic cells. In good correlation, transplants of β-catenin-deficient chondrocytes into athymic mice persisted for a longer period of time and resisted replacement by bone compared to control wild-type chondrocytes. In contrast, a β-catenin signaling stimulator increased cell death in control chondrocytes. Immunohistochemical analysis revealed that the amount of detectable β-catenin in cartilage cells of osteochondromas obtained from hereditary multiple exostoses patients was much lower than that in hypertrophic chondrocytes in normal human growth plates. The findings in our study indicate that loss of β-catenin expression in chondrocytes induces periosteal chondroma-like masses and may be linked to, and cause, the persistence of cartilage caps in osteochondromas.
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Registered trials
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