Lectin Potentiation of BCG-Contact-Medlated Antitumor Action 1,2

contact-mediated antitumor action when both Con A (10 Ilg) and BCG (50 Ilg) were injected with fibrosarcoma cells (5Xl0·) into inbred Swiss mice. BCG (50 Ilg) alone had no antitumor effect. The Con A-potentiated BCG-contact-mediated phenomenon was shown to be immunologically mediated, inasmuch as tumors developed in immunosuppressed mice inoculated with tumor cells mixed with Con A and BCG. The same dose of 50 Ilg BCG was effective in controlling the growth of 10 · fibrosarcoma cells in the presence of Con A. The specific inhibitor of Con A, a-methyl D-mannoside, abrogated the potentiation of the BCG effect seen with Con A. Con A also increased the antitumor effect of BCG in sarcoma 180 ascites tumor. Another lectin, peanut agglutinin, also induced an antitumor effect in the presence of BCG only when the tumor cells were treated with Vibrio cboteree neuramin-idase.-JNCI 65: 909-912, 1980. The growth of syngeneic transplants of experimental tumors may be inhibited by inoculation of tumor cells mixed with certain strains of BCG (1-4). In clinical situations also, close contact of BCG with the tumor has been shown to be essential for tumor inhibition (5). In most systems reduction in the number of BCG organisms for a given tumor cell eventually eliminated the antitumor effect (4, 6). These studies (1-6) indicate that an intimate association of BCG with the tumor cells and an adequate number of BCG organisms are prerequisites for achieving tumor rejection. However, little attention has been devoted to the interaction between tumor target cell, BCG organisms, and the effector killer cell (lymphocytes or macrophages). Be-cause saccharides are available both on the mammalian cell membrane and bacterial cell wall, we used lectins as a possible ligand to-mcrease the interaction between tumor cell, BCG, and effector cell. In the present studies we have brought down considerably the effec-tive dose of BCG required to suppress a murine fibro-sarcoma by the use of the lectins Con A and PNA in conjunction with BCG