Osteofibrous dysplasia

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Soft Tissue and Bone Tumours (Who Classification, 5th ed.)

Primary Author(s)*

Kathleen Schieffer, PhD, FACMG

WHO Classification of Disease

Structure Disease
Book Soft Tissue and Bone Tumours (5th ed.)
Category Bone tumours
Family Other mesenchymal tumours of bone
Type Osteofibrous dysplasia
Subtype(s) N/A

Related Terminology

Acceptable N/A
Not Recommended Ossifying fibroma of long bones; Kempson–Campanacci lesion

Gene Rearrangements

Driver Gene Fusion(s) and Common Partner Genes Molecular Pathogenesis Typical Chromosomal Alteration(s) Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
N/A N/A N/A N/A N/A N/A N/A N/A

Individual Region Genomic Gain/Loss/LOH

Chr # Gain, Loss, Amp, LOH Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size] Relevant Gene(s) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
N/A N/A N/A N/A N/A N/A N/A

Characteristic Chromosomal or Other Global Mutational Patterns

Chromosomal Pattern Molecular Pathogenesis Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
N/A N/A N/A N/A N/A N/A

Gene Mutations (SNV/INDEL)

Gene Genetic Alteration Tumor Suppressor Gene, Oncogene, Other Prevalence -

Common >20%, Recurrent 5-20% or Rare <5% (Disease)

Diagnostic, Prognostic, and Therapeutic Significance - D, P, T   Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes
MET Exon 14 skipping (activating) Oncogene Recurrent D No Exon 14 of MET encodes a regulatory domain which signals for polyubiquitination and degradation of MET following phosphorylation of Tyr1003. However, exon 14 skipping events result in a loss of Tyr1003, impaired degradation, and oncogenic activation of MET signaling.[1][2] Of note, only relatively few germline cases have been reported in the literature and a somatic alteration (p.Tyr1003Ser) has been reported in a single sample.[2] The prevalence may be under-represented.

Note: A more extensive list of mutations can be found in cBioportal, COSMIC, and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.

Epigenomic Alterations

None

Genes and Main Pathways Involved

Gene; Genetic Alteration Pathway Pathophysiologic Outcome
MET; Activating exon 14 skipping RAS/MAPK, PI3K/AKT signaling Increased cell growth and proliferation[1]

Genetic Diagnostic Testing Methods

DNA sequencing may identify variation resulting in exon 14 skipping. Transcriptome analysis would be recommended to confirm alternative splicing.

Familial Forms

Germline alterations in MET which result in exon 14 skipping have been shown to be associated with familial osteofibrous dysplasia.[2]

Additional Information

Not applicable

Links

None

References

  1. 1.0 1.1 Ghosh, Promita; et al. (2025-09-09). "Mechanistic insights into MET exon 14 skipping mutations and their role in tumor progression". Biochemical Society Transactions: BST20253091. doi:10.1042/BST20253091. ISSN 1470-8752. PMID 40924941 Check |pmid= value (help).
  2. 2.0 2.1 2.2 Gray, Mary J.; et al. (2015-12-03). "Mutations Preventing Regulated Exon Skipping in MET Cause Osteofibrous Dysplasia". American Journal of Human Genetics. 97 (6): 837–847. doi:10.1016/j.ajhg.2015.11.001. ISSN 1537-6605. PMC 4678433. PMID 26637977.


Notes

*Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the Associate Editor or other CCGA representative.  When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.

Prior Author(s): *Citation of this Page: “Osteofibrous dysplasia”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 10/22/2025, https://ccga.io/index.php/STBT5:Osteofibrous dysplasia.