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Tumorigenicity and Oncogene Expression in Pediatric Cancers¹

Division of Hematology-Oncology, Children's Hospital of Los Angeles and Department of Microbiology, USC School of Medicine [S. R. P., G. R. J., B. E. W.], Los Angeles, California 90033, and Corporate Research Division, Procter and Gamble Company, Miami Valley Laboratories, Cincinnati, Ohio 45239-8707 [C-J. D.]

Cytogenetic and epidemiological studies of pediatric cancers have implicated a loss of genetic information in the development of these tumors. In contrast, other studies have shown that activation of endogenous oncogenes is a common event in these cancer cells. The technique of somatic cell hybridization provides a model for investigating the interaction between loss of genetic elements and oncogene activation in pediatric cancers. A variety of human-human cell hybrids were formed between a tumorigenic adult carcinoma and representative tumorigenic pediatric cell lines. All hybrid cells were completely suppressed for tumor-forming ability when assayed in nu/nu (nude) mice. When the expression of the N-myc, c-myc, and sis oncogenes and tumorigenicity were examined in the same hybrid cells, no correlation was found, suggesting that the expression of these oncogenes in these hybrid cells did not appear to be controlled by putative "tumor suppressor" genes. Thus, tumorigenicity behaves as a recessive genetic trait in pediatric cancers. Furthermore, different genetic elements may be lost during tumor development of adult cancers as opposed to pediatric cancers.

¹ This work was funded by USPHS Grant S07RR05469-23 from the National Cancer Institute and by the Clayton Foundation Molecular Biology Program.

² Supported by USPHS Training Grant 2T32AI07078-07 from the NIH.

³ Present address: Children's Hospital Research Foundation, Cincinnati, OH 45229.

⁴ To whom requests for reprints should be addressed.

Received 10/ 8/87. Revised 1/21/88. Accepted 2/19/88.