MY-1, a fraction extracted from BCG and composed of 70.0%
DNA and 28.0%
RNA, was examined for its antitumor activity against 9 different syngeneic mouse
tumors.
Tumor regression was induced in almost all of the mice bearing any of five kinds of solid
tumors by repeated
intralesional injections of 100 micrograms MY-1. When cells of some
tumors were inoculated intradermally together with MY-1,
tumor growth was suppressed, lung
metastases were inhibited, and the survival times of mice bearing 1 of 3 leukemic
tumors were prolonged. Repeated sc
injections with MY-1 in sites remote from
tumor cell inoculation or repeated iv
injections were more or less effective against three kinds of solid
tumors. Mice inoculated with
Lewis lung carcinoma cells in a hind footpad and whose legs were amputated 9 days later were given iv or sc
injections of MY-1 every other day (8 times in total), resulting in substantial prolongation of survival. No direct cytotoxicity of MY-1 for these
tumors could be shown in three kinds of experiments, which indicates that the antitumor mechanism of MY-1 is host mediated. MY-1 was equally effective in mice with or without presensitization with BCG, whereas BCG was much more effective in BCG-sensitized mice. This finding suggests that a delayed-type
hypersensitivity reaction elicited by BCG
protein is not required for the antitumor activity of MY-1.