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Intraclonal Conversion from Papilloma to Carcinoma in the Skin of Pgk-1^a/Pgk-1^b Mice Treated by a Complete Carcinogenesis Process or by an Initiation-Promotion Regimen¹

Institute for Cancer Research, Osaka University Medical School, Nakanoshima 4-3-57, Kita-ku, Osaka 530, Japan

Skin tumors were produced by either a complete carcinogenesis process or an initiation-promotion regimen in C57BL/6 x C3H/HeHa F₁-Pgk-1^b/Pgk-1^a mice which carried X-chromosome inactivation mosaicism for the phosphoglycerate kinase gene. In the complete carcinogenesis process, 200 nmol of 7,12-dimethylbenza(a)anthracene were applied once weekly; in the initiation-promotion regimen, a single application of 200 nmol of 7,12-dimethylbenz(a)anthracene was followed by twice weekly applications of 17 nmol of 12-O-tetradecanoylphorbol-13-acetate. Most papillomas produced by either procedure contained only one type of phosphoglycerate kinase, suggesting the monoclonal origin of papillomas. When the carcinoma developed at the same place where the papilloma was observed, the phosphoglycerate kinase type of most carcinomas was consistent with that of the original papillomas. This suggests that the malignant tumor develops as a result of the intraclonal conversion from the benign tumor.

¹ This work was supported by Grants-in-Aid for cancer research from the Ministry of Education, Science, and Culture; the Ministry of Health and Welfare; and the Princess Takamatsu Cancer Research Fund.

² To whom requests for reprints should be addressed.

Received 2/29/84. Accepted 6/ 4/84.