AN ALTERATION IN TUMOR HISTOCOMPATIBILITY INDUCED BY NEURAMINIDASE

Abstract

The TA3 tumor is characterized by a heavy sialomucin cell surface coating demonstrable by specific histochemical staining. Enzymatic removal of sialic acid from the tumor cells resulted in an apparent increase in the specificity of this tumor. With neuraminidase treatment, 3000 TA3 cells produced lethal takes in only 6 ± 4% of allogeneic C3H hosts, compared with 56 ± 5% lethal takes observed in untreated C3H controls. Simple destruction of tumor cells by neuraminidase was unlikely since syngeneic strain A hosts regularly became distended after tumor injection although regression often occurred later. Nonspecific stimulation of the reticuloendothelial system was also unlikely since treatment of hosts with complete Freund's adjuvant was ineffective. Studies of tumor rejectors showed that a solid immunity could be obtained to an earlier, more specific TA3 line but could not be achieved with the nonspecific TA3 line. Results obtained so far are consistent with an explanation in terms of masking of isoantigens at the tumor cell surface with sialomucin.