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Amplification of c-myc oncogene and absence of c-Ha-ras point mutation in human bone sarcoma
C Barrios1, J S Castresana, J Ruiz
1Department of Orthopedics, Karolinska Hospital, Stockholm, Sweden.
Abstract:
The genomic organization of four oncogenes, c-myc, c-myb, c-Ha-ras, and v-fms, was analyzed in 21 patients with malignant bone tumors. Amplification of the c-myc proto-oncogene without rearrangement was the sole abnormality detected in four tumors: two chondrosarcomas, one osteosarcoma, and one lymphoma of bone. DNA hybridizations with c-myb, c-Ha-ras, and v-fms probes disclosed no structural gene abnormalities. Point mutations at the 12th codon of the c-Ha-ras gene were investigated with the polymerase chain reaction technique; no alterations were detected. The observed amplification of the c-myc there was not related to histologic type, grade, surgical stage, or ploidy level of the tumors. The results indicated that c-myc amplification, presumed to be involved in the development of malignancy in a variety of solid tumors, is encountered sporadically in malignant bone tumors; however, this occurs without relation to common histopathologic features. The clinical significance of oncogene amplification in bone sarcoma remains to be established.
Insights
Amplification of the c-myc proto-oncogene was found in some malignant bone tumors but not others. This genetic change, c-myc amplification, appears sporadically and is not linked to tumor type or stage.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Oncogenes play a role in cancer development.
- The genomic organization of oncogenes in malignant bone tumors is not fully understood.
- Previous research suggests c-myc amplification is involved in various solid tumors.
Purpose of the Study:
- To analyze the genomic organization of four key oncogenes (c-myc, c-myb, c-Ha-ras, v-fms) in malignant bone tumors.
- To investigate the presence and nature of genetic abnormalities in these oncogenes.
- To determine the relationship between oncogene alterations and tumor characteristics.
Main Methods:
- Analysis of genomic DNA from 21 patients with malignant bone tumors.
- DNA hybridization using probes for c-myb, c-Ha-ras, and v-fms.
- Polymerase chain reaction (PCR) to detect point mutations in the c-Ha-ras gene.
- Assessment of c-myc proto-oncogene amplification and rearrangement.
Main Results:
- c-myc proto-oncogene amplification without rearrangement was detected in four tumors (two chondrosarcomas, one osteosarcoma, one bone lymphoma).
- No structural gene abnormalities were found for c-myb, c-Ha-ras, or v-fms.
- No point mutations at the 12th codon of the c-Ha-ras gene were detected.
- c-myc amplification was not associated with tumor histologic type, grade, surgical stage, or ploidy level.
Conclusions:
- c-myc amplification occurs sporadically in malignant bone tumors.
- This amplification is not related to common histopathologic features of bone tumors.
- The clinical significance of oncogene amplification in bone sarcoma requires further investigation.