When cell suspensions of Rous sarcoma and its variant strain, 14(d)7, were transplanted into nontreated hamsters, tumors always regressed within 10 days. However, in cortisone-treated hamsters, tumors grew and maintained their sizes for longer than 3 weeks. During these periods, a high virus titer persisted.

Transplantation of hamster-grown tumors into conditioned hamsters was difficult after two generations. However, when normal chick embryonic tissues were added to them, further transplantation became possible. When normal chick embryonic tissues were added to extracts of hamster-grown tumors, tumors also developed in conditioned hamsters. In these cases, virus-infected chick embryonic tissues were transformed into sarcoma. Thus, 14(d)7 sarcoma was maintained in hamsters for nine generations during a period of more than 100 days. When hamster embryo was ground together with chicken sarcoma extract and injected into newborn or cortisone-treated adult hamsters, no malignant changes were observed in these tissues.

Rous sarcoma and the 14(d)7 strain grew in conditioned hamsters to far smaller sizes than they did in chickens. However, the virus yield in the former was higher than in the latter.

The mode of virus action in the growth of tumors in cortisone-treated hamsters was discussed in correlation with the role of infectious and noninfectious forms of viruses in the proliferation of malignant tumor cells.


Dedicated to the late Dr. F. Duran-Reynals, in whose laboratory this work was carried out.

Presented at the 17th General Meeting of the Japanese Cancer Association, Nov. 9, 1958.

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