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Detection of Point Mutations in N-ras and K-ras Genes of Human Embryonal Rhabdomyosarcomas Using Oligonucleotide Probes and the Polymerase Chain Reaction¹

Section of Chemical Carcinogenesis [M. R. S., C. S. C.], Chester Beatty Laboratories, Institute of Cancer Research, Fulham Road, London SW3 6JB; Section of Pathology [B. A. G.], Haddow Laboratories, Institute of Cancer Research, 15 Cotswold Road, Belmont, Sutton, Surrey SM2 5NG; and Department of Histopathology [C. F.], Royal Marsden Hospital, Fulham Road, London SW3 6JJ, United Kingdom

Previous studies have demonstrated that genes of the ras family (H, K, and N) can be activated by point mutations at codons 12, 13, and 61. In the present study we have used oligonucleotide probes corresponding to these regions to assess the role of ras gene mutations in the genesis of human rhabdomyosarcoma. To increase the sensitivity of this method the appropriate regions of the three ras genes were first amplified using the polymerase chain reaction. The results show that 35% (5/14) embryonal rhabdomyosarcomas investigated contain mutations in the N-ras or K-ras genes. Thus ras gene mutation is implicated in the development of mesenchymal and embryonal tumors in addition to its previously documented role in epithelial and hematological neoplasia.

¹ This work was supported by grants from the Medical Research Council and Cancer Research Campaign.

² MRC Training Fellow.

Received 4/27/89. Revised 8/ 7/89. Accepted 8/15/89.

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