ArticleOncogene2012
Secondary peripheral chondrosarcoma evolving from osteochondroma as a result of outgrowth of cells with functional EXT.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- A Systematic Review of Adjuvant Chemotherapy in Localized Dedifferentiated Chondrosarcoma.Current oncology (Toronto, Ont.) · 2024Pooled it
- Chondrosarcoma: A comprehensive review of tumor biology, clinical behavior, and therapeutic advances.Cancer treatment reviews · 2026Review
- The Role of AXL Signaling and MutantCancers · 2026Review
- Chondrosarcoma organoids reveal SHH pathway activation driven by PTCH1 and BCOR alterations.Scientific reports · 2025Article
- Management of Lower Extremity Deformity in Children with Hereditary Multiple Exostoses.Journal of the Pediatric Orthopaedic Society of North America · 2025Review
- Advances in the Molecular Biology of Chondrosarcoma for Drug Discovery and Precision Medicine.Cancers · 2025Review
- Dedifferentiated Chondrosarcoma: Diagnostic Controversies and Emerging Therapeutic Targets.Current oncology reports · 2023Review
- Biology and Management of High-Grade Chondrosarcoma: An Update on Targets and Treatment Options.International journal of molecular sciences · 2023Review
- Article
- Clinical survey of a pedigree with hereditary multiple exostoses and identification of EXT‑2 gene deletion mutation.Molecular medicine reports · 2022Article
- An update on the imaging of diaphyseal aclasis.Skeletal radiology · 2021Review
- Review
- Mutation spectrum of EXT1 and EXT2 in the Saudi patients with hereditary multiple exostoses.Orphanet journal of rare diseases · 2021Article
- Identification of Novel EXT Mutations in Patients with Hereditary Multiple Exostoses Using Whole-Exome Sequencing.Orthopaedic surgery · 2020Article
- Review
- [Cartilage tumors: morphology, genetics, and current aspects of target therapy].Der Pathologe · 2020Review
- Nicotinamide Phosphoribosyl Transferase Is Increased in Osteosarcomas and Chondrosarcomas Compared to Benign Bone and Cartilage.Anticancer research · 2019Article
- Biology of Bone Sarcomas and New Therapeutic Developments.Calcified tissue international · 2018Review
- Chondrosarcoma: biology, genetics, and epigenetics.F1000Research · 2018Review
- Advances in the pathogenesis and possible treatments for multiple hereditary exostoses from the 2016 international MHE conference.Connective tissue research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary peripheral chondrosarcoma is the result of malignant transformation of a pre-existing osteochondroma, the most common benign bone tumor. Osteochondromas are caused by genetic abnormalities in EXT1 or EXT2: homozygous deletion of EXT1 characterizes sporadic osteochondromas (non-familial/solitary), and germline mutations in EXT1 or EXT2 combined with loss of heterozygosity define hereditary multiple osteochondromas. While cells with homozygous inactivation of EXT and wild-type cells shape osteochondromas, the cellular composition of secondary peripheral chondrosarcomas and the role of EXT in their formation have remained unclear. We report using a targeted-tiling-resolution oligo-array-CGH (array comparative genomic hybridization) that homozygous deletions of EXT1 or EXT2 are much less frequently detected (2/17, 12%) in sporadic secondary peripheral chondrosarcomas than expected based on the assumption that they originate in sporadic osteochondromas, in which homozygous inactivation of EXT1 is found in ~80% of our cases. FISH with an EXT1 probe confirmed that, unlike sporadic osteochondromas, cells from sporadic secondary peripheral chondrosarcomas predominantly retained one (hemizygous deleted loci) or both copies (wild-type) of the EXT1 locus. By immunohistochemistry, we confirm the presence of cells with dysfunctional EXT1 in sporadic osteochondromas and show cells with functional EXT1 in sporadic secondary peripheral chondrosarcomas. These immuno results were verified in osteochondromas and secondary peripheral chondrosarcomas in the setting of hereditary multiple osteochondromas. Our data therefore point to a model of oncogenesis in which the osteochondroma creates a niche in which wild-type cells with functional EXT are predisposed to acquire other mutations giving rise to secondary peripheral chondrosarcoma, indicating that EXT-independent mechanisms are involved in the pathogenesis of secondary peripheral chondrosarcoma.
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