This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gemma, A. Articles by Shimosato, Y. Search for Related Content PubMed PubMed Citation Articles by Gemma, A. Articles by Shimosato, Y.

myc Family Gene Abnormality in Lung Cancers and Its Relation to Xenotransplantability¹

Pathology [A. G., T. N., M. N., M. G., Y. S.] and Oncogene [M. S., T. S.] Divisions, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku 104, Tokyo; and Department of Clinical Pathology [A. G., H. N.], Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113, Japan

In order to study the relationship between tumor transplantability to the nude mouse and abnormality of the myc family genes (c-myc, N-myc, L-myc) in human primary lung cancers, 32 various lung cancers were analyzed for abnormality of the myc family genes by Southern blot hybridization, and were transplanted s.c. into nude mice. Southern blot analysis showed that four non-small cell carcinomas and three small cell carcinomas had amplified c-myc and L-myc genes, respectively. Allelic deletion of the L-myc gene was observed in seven cancers, of which two also had an additional band of the c-myc gene or amplification of the L-myc gene. No abnormality of the N-myc gene was observed in this series. Of 13 cancers with abnormality of the myc family genes, 11, including all tumors with myc gene amplification, were transplantable to nude mice. Of 19 tumors without any abnormalities of the myc family genes, however, only five were transplantable to nude mice (P < 0.005). These results indicate that abnormality of the myc family genes, especially gene amplification, might promote tumorigenic ability in xenotransplantation of lung cancers and this phenomenon might be closely related to the function of the myc gene.

¹ This work was supported by Grants-in-Aid for Cancer Research from the Ministry of Health and Welfare, Japan.

² To whom requests for reprints should be addressed.

Received 3/25/88. Revised 7/15/88. Accepted 7/27/88.