scholarly journals Killing tumor cells through their surface β2-microglobulin or major histocompatibility complex class I molecules

Cancer ◽  
2010 ◽  
Vol 116 (7) ◽  
pp. 1638-1645 ◽  
Author(s):  
Jing Yang ◽  
Qing Yi
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Tumor Cells ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Β2 Microglobulin ◽  
Histocompatibility Complex

Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene

1988 ◽  
Vol 8 (4) ◽  
pp. 1857-1861
Author(s):  
K Tanaka ◽  
E Gorelik ◽  
M Watanabe ◽  
N Hozumi ◽  
G Jay
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Tumor Cells ◽  
Human Cancer ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
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.

scholarly journals Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.

1988 ◽  
Vol 8 (4) ◽  
pp. 1857-1861 ◽  
Author(s):  
K Tanaka ◽  
E Gorelik ◽  
M Watanabe ◽  
N Hozumi ◽  
G Jay
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Tumor Cells ◽  
Human Cancer ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
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.

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