• DOI:10.1093/JNCI/74.3.681
• Corpus ID: 34868694

Antitumor activity of the DNA fraction from Mycobacterium bovis BCG. II. Effects on various syngeneic mouse tumors.

@article{Shimada1985AntitumorAO,
  title={Antitumor activity of the DNA fraction from Mycobacterium bovis BCG. II. Effects on various syngeneic mouse tumors.},
  author={Shizuo Shimada and Osamu Yano and Hiroko Inoue and Etsuro Kuramoto and T Fukuda and H. Yamamoto and Tetsuro Kataoka and Tohru Tokunaga},
  journal={Journal of the National Cancer Institute},
  year={1985},
  volume={74 3},
  pages={
          681-8
        }
}

• S. Shimada, O. Yano, +5 authors T. Tokunaga
• Published 1 March 1985
• Biology, Medicine, Chemistry
• Journal of the National Cancer Institute

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.