Volume 11, Issue 4 pp. 556-563
Article
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Amplification of c-myc oncogene and absence of c-Ha-ras point mutation in human bone sarcoma

Dr. Carlos Barrios

Corresponding Author

Dr. Carlos Barrios

Department of Orthopeaics, Karolinska Hospital, Stocholm, Sweden

Orthopedics and Trauma Institute, Clínica Quirón, Blasco Ibañez 14, 46010 Valencia, SpainSearch for more papers by this author
Javier S. Castresana

Javier S. Castresana

Molecular Neuro-Oncology Laboratory, Massachusetts General Hospital, Boston, Massachusetts, U.S.A.

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Juan Ruiz

Juan Ruiz

Department of Tumor Pathology, Karolinska Hospital, Stocholm, Sweden

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Andris Kreicbergs

Andris Kreicbergs

Department of Orthopeaics, Karolinska Hospital, Stocholm, Sweden

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First published: July 1993
Citations: 30

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.

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