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COPS3 amplification and clinical outcome in osteosarcoma.

Taiqiang Yan1, Jay S Wunder, Nalan Gokgoz

  • 1Fred A. Litwin Centre for Cancer Genetics, Mount Sinai Hospital, and University Musculoskeletal Oncology Unit, Toronto, Ontario, Canada.

Cancer
|March 17, 2007
PubMed
Summary

Amplification of the COPS3 gene in osteosarcoma is linked to larger tumors and a higher risk of metastasis. This suggests COPS3 may act as an oncogene, potentially worsening patient prognosis.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • High-grade osteosarcoma frequently shows amplification of genes on chromosome 17p11.2, including COPS3.
  • COPS3 encodes a protein involved in regulating the P53 tumor suppressor, suggesting a role in osteosarcoma development.

Purpose of the Study:

  • To investigate the relationship between COPS3 gene amplification, P53 mutations, and patient outcomes in osteosarcoma.
  • To determine if COPS3 amplification is a predictive marker for prognosis in high-grade osteosarcoma.

Main Methods:

  • Quantitative real-time polymerase chain reaction (PCR) was used to assess COPS3 copy number in 155 osteosarcoma tumors.
  • Univariate and multivariate survival analyses were conducted to evaluate the impact of COPS3 amplification on patient outcomes.

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Last Updated: Jul 16, 2026

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Main Results:

  • COPS3 amplification was found in 31% of osteosarcomas and associated with larger tumor size.
  • COPS3 amplification showed a trend towards shorter time to metastasis in univariate analysis, but this was not significant in multivariate analysis.
  • COPS3 amplification and P53 mutations often co-occurred in osteosarcoma tumors.

Conclusions:

  • COPS3 is identified as a likely target of the 17p11.2 amplicon in osteosarcoma.
  • Increased COPS3 copy number may contribute to osteosarcoma progression and an unfavorable prognosis.
  • COPS3 may function as an oncogene in the development of osteosarcoma.