Phenotypic instability of mouse melanomas after propagation in vivo and in vitro.

This study was designed to evaluate the phenotypic stability of the carcinogen-induced JB/MS and JB/RH melanomas. The JB/MS melanoma maintained its original slow-growing melanotic phenotype during in vivo passage over a 2-yr period. However, both melanin production and tumorigenicity decreased rapidly after propagation of JB/MS cells in vitro. The JB/RH melanoma became essentially amelanotic after the second transplantation in vivo. Cultured JB/RH cells produced tumors identical to those obtained by transplantation of JB/RH tumor fragments. However, after propagation in vitro for 2 yr, the JB/RH cell line decreased in tumorigenicity, requiring 10 times as many cells to produce tumors in C57BL/6 mice as did the original cell line. The JB/RH melanoma was highly immunogenic in syngeneic C57BL/6 mice, and passage of JB/RH cells through immunized mice resulted in tumors that were significantly more tumorigenic in normal mice than were JB/RH cells that had been passed through either nude or sublethally irradiated mice. These results indicate that, in studies of primary mouse melanomas, it is essential to: (a) limit the number of tumor passages; (b) choose methods of propagation that will preserve the original phenotype; and (c) distinguish those properties produced by technical manipulation from those produced by true tumor progression.

A naturally occurring intestinal mouse adenovirus infection associated with negative serologic findings.

Large basophilic intranuclear inclusions were observed in the intestinal epithelium of clinically normal mice. Electron micrographs of the inclusions showed them to be caused by an adenovirus, even though serological testing for mouse adenoviruses in a complement fixation test using the FL strain of mouse adenovirus yielded no titers. A diagnosis of an adenovirus infection resembling that caused by the K87 strain was made.