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Low level amplification of c-sis and c-myc in a spontaneous osteosarcoma model

D T Kochevar1, J Kochevar, L Garrett

  • 1Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine, Texas A and M University, College Station 77843.

Cancer Letters
|September 1, 1990
PubMed

Insights

Canine and human osteosarcoma share similarities. This study found significant amplification of c-sis and c-myc protooncogenes in canine osteosarcoma tumors, suggesting their role in cancer development.

Area of Science:

  • Oncology
  • Genetics
  • Comparative Pathology

Background:

  • Canine and human osteosarcomas exhibit striking clinical, radiological, and pathological resemblances.
  • Protooncogene alterations are implicated in various cancers, including osteosarcoma.

Purpose of the Study:

  • To investigate the amplification and expression of specific protooncogenes (c-sis, c-myc, N-myc, c-H-ras) in canine osteosarcoma.
  • To compare these genetic alterations with those found in human osteosarcoma and normal tissues.

Main Methods:

  • DNA extraction from canine osteosarcoma tissues and normal canine controls.
  • Analysis of protooncogene amplification using molecular techniques.
  • Examination of DNA and RNA from cultured canine and human osteosarcoma and fibroblast cell lines.
  • Immunostaining for the sis gene product (PDGF B).

Main Results:

  • Statistically significant amplification of c-sis and c-myc protooncogenes was observed in canine tumor tissues compared to normal controls (P < 0.05).
  • Low levels of c-myc and c-sis DNA amplification were detected in cultured canine osteosarcoma cells versus canine fibroblasts.
  • Similar levels and patterns of PDGF B expression were found in both human and canine osteosarcoma tissues.

Conclusions:

  • The findings suggest that c-sis and c-myc protooncogene amplification plays a role in canine osteosarcoma development.
  • The similarities in protooncogene alterations and PDGF B expression reinforce the value of canine osteosarcoma as a model for human disease.

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