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Mutational activation of ras genes is absent in pediatric osteosarcoma
F Antillón-Klüssmann1, M García-Delgado, I Villa-Elízaga
1Department of Pediatrics, School of Medicine, Universidad de Navarra, Pamplona, Spain.
Abstract:
Activation of ras oncogenes is found in human cancers; overall it is observed in 15% of all neoplasms. The purpose of this study was to assess the extent of involvement of ras oncogenes in osteosarcoma. Tumor samples from a series of 49 pediatric patients diagnosed with osteosarcoma and treated at our institution were evaluated. Paraffin-embedded tumor samples from diagnostic biopsies, from tumor en bloc resection tissue after neoadjuvant chemotherapy, and samples from metastases were examined in search of point mutations in H, K, and N-ras genes at codons 12 and 61 by means of polymerase chain reaction (PCR), slot-blotting, and radioactive labeled specific DNA probes. A total of 92 archival samples were studied. No point mutations activating these genes were found. These findings suggest that the activation by point mutations at codons 12 and 61 of the H, K, and N-ras genes does not play a role in the pathogenesis of human osteosarcoma. Since no point mutations in codons 12 and 61 were detected, it was not possible to establish any correlation between the ras genes and clinical or histologic findings.
Insights
Ras oncogene mutations are common in cancers but not found in pediatric osteosarcoma. This study found no evidence that ras gene point mutations at codons 12 and 61 contribute to osteosarcoma development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ras oncogenes are frequently activated in human cancers, present in approximately 15% of all neoplasms.
- Understanding the role of ras oncogenes in specific cancer types, like osteosarcoma, is crucial for targeted therapies.
Purpose of the Study:
- To investigate the involvement of ras oncogenes in the pathogenesis of human osteosarcoma.
- To determine if point mutations in H, K, and N-ras genes at codons 12 and 61 are present in osteosarcoma samples.
Main Methods:
- Analysis of 92 archival paraffin-embedded tumor samples from 49 pediatric osteosarcoma patients.
- Utilized polymerase chain reaction (PCR), slot-blotting, and radioactive labeled DNA probes to detect point mutations.
- Examined samples from diagnostic biopsies, post-neoadjuvant chemotherapy resection tissue, and metastases.
Main Results:
- No activating point mutations were detected in the H, K, or N-ras genes at codons 12 and 61.
- The study found no correlation between ras gene mutations and clinical or histological findings in osteosarcoma.
Conclusions:
- Activation of H, K, and N-ras genes through point mutations at codons 12 and 61 does not appear to be a significant factor in the development of human osteosarcoma.
- Further research may be needed to explore other potential genetic alterations involved in osteosarcoma pathogenesis.