Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.
Transfection of a functional major histocompatibility complex class I gene into certain tumor cells, induced by oncogenic viruses or chemical carcinogens, can effectively abrogate their tumorigenic activity. Since experimentally induced tumors possess strong tumor-specific transplantation antigens, expression of cell surface class I antigens may present the tumor cells to appropriate immune effector cells. Most spontaneously arising tumors do not possess tumor-specific transplantation antigens, and their tumorigenicity may not be affected by the expression of a transfected class I gene. We demonstrate that the poorly immunogenic B16-BL6 melanoma can be rendered nontumorigenic in syngeneic mice by the expression of the class I H-2K antigen but not the class II I-A antigen. Furthermore, the poorly tumorigenic, class I-expressing B16-BL6-transfected cells can effectively immunize syngeneic C57BL/6 mice against the highly tumorigenic, class I-deficient B16-BL6 parental cells. Our success in experimentally manipulating the tumorigenicity of a spontaneously derived neoplasm offers hope for a potential modality for the effective treatment of human cancer.
Tanaka
K
K
Laboratory of Molecular Virology, National Cancer Institute, Bethesda, Maryland 20892.
Gorelik
E
E
Watanabe
M
M
Hozumi
N
N
Jay
G
G
D000818:Animals; D005805:Genes, MHC Class I; D006084:Graft Rejection; D008546:Melanoma, Experimental / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D009368:Neoplasm Transplantation; D014158:Transcription, Genetic; D014162:Transfection; D014185:Transplantation, Isogeneic