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Updated: Jun 2, 2026

Injection of Syngeneic Murine Melanoma Cells to Determine Their Metastatic Potential in the Lungs
Published on: May 24, 2016
Rejection of murine melanoma-cells transfected with the intercellular-adhesion molecule-1 gene
P Chen1, V Shreedhar, H Ananthaswamy
1UNIV TEXAS,MD ANDERSON CANC CTR,DEPT IMMUNOL,HOUSTON,TX 77030.
The effects of intercellular adhesion molecule-1 (ICAM-1) expression on-tumor rejection and induction of antitumor immunity in a murine melanoma system was studied. K1735 melanoma cells genetically engineered to express the murine ICAM-1 gene were rejected in immunocompetent hosts, and that this rejection was mediated by CD4(+) as well as by CD8(+) T lymphocytes. We also found that ICAM-1 transfected tumor cells provided costimulatory signals to both CD4(+) and CD8(+) T cells in vitro. In addition, immunization of mice with K1735-ICAM-1 transfectants induced protective immunity against the parental ICAM-1-negative tumor. Our findings suggest that ICAM-1 expression on nonimmunogenic tumor cells causes tumor rejection and augments tumor-specific immunity.
The effects of intercellular adhesion molecule-1 (ICAM-1) expression on-tumor rejection and induction of antitumor immunity in a murine melanoma system was studied. K1735 melanoma cells genetically engineered to express the murine ICAM-1 gene were rejected in immunocompetent hosts, and that this rejection was mediated by CD4(+) as well as by CD8(+) T lymphocytes. We also found that ICAM-1 transfected tumor cells provided costimulatory signals to both CD4(+) and CD8(+) T cells in vitro. In addition, immunization of mice with K1735-ICAM-1 transfectants induced protective immunity against the parental ICAM-1-negative tumor. Our findings suggest that ICAM-1 expression on nonimmunogenic tumor cells causes tumor rejection and augments tumor-specific immunity.
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