Abstract Somatic cell hybrid lines were obtained by Sendai virus mediated fusion of a highly tumorigenic variant of L-cell subline A9 of C3H mouse origin (A9HT) with two CBA mouse mammary carcinomas (SBfnHA and SBfnHC) that had been inoculated into CBAT6 mice. Hybridity was confirmed by the presence of biarmed marker chromosomes from the A9HT parent, and the total chromosome number, which in both hybrids (SBfnHA/A9HT and SBfnHC/A9HT) approximated the sum of the parental chromosomes. The absence of the T6 marker in both the hybrids confirmed that fusion was not between a stroma cell from CBAT6 mice and A9HT. Both hybrids showed spindle cell carcinoma morphology. Complement dependent cytotoxicity assays revealed that SBfnHA and A9HT expressed the MTV-associated antigens including one major structural component, gp52 and the MuLV structural components gp71. and p30 on the cell-surface, while SBfnHC expressed only gp71. The hybrid line SBfnHA/A9HT lost the surface expression of MTV gp52 and MuLVp30, and there was also decreased expression of gp71 in comparison with SBfnHA. In contrast, in SBfnHC/A9HT there was increased expression of gp71 over that of SBfnHC. All parental and hybrid lines had unchanged sensitivity to the cytotoxic effect of anti-H-2 k sera. Immunization of CBA mice with heavily irradiated either syngeneic SBfnHA or hybrid SBfnHA/A9HT cells, followed by challenge with viable SBfnHA cells revealed that SBfnHA was a highly immunogenic tumor, while the hybrid line SBfnHA/A9HT decreased in the immunogenicity of the parental SBfnHA line. On the other hand, immunization of CBA mice with heavily irradiated either syngeneic SBfnHC or hybrid SBfnHC/A9HT cells, followed by challenge with viable SBfnHC cells showed that SBfnHC/A9HT slightly increased the very low immunogenicity of the parental SBfnHC. These results are consistent with the possibility that MTV-and MuLV-associated cell-surface antigens influence the immunogenicity of CBA mammary carcinomas.