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10.1111/j.1349-7006.1996.tb00284.x

http://scihub22266oqcxt.onion/10.1111/j.1349-7006.1996.tb00284.x
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C5921150!5921150!8698622
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suck abstract from ncbi


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pmid8698622      Jpn+J+Cancer+Res 1996 ; 87 (7): 724-9
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  • Rejection of Mouse Renal Cell Carcinoma Elicited by Local Secretion of Interleukin?2 #MMPMID8698622
  • Hara I; Hotta H; Sato N; Eto H; Arakawa S; Kamidono S
  • Jpn J Cancer Res 1996[Jul]; 87 (7): 724-9 PMID8698622show ga
  • We introduced the interleukin?2 (IL?2) gene into mouse renal cell carcinoma (RenCa) in order to examine the mechanism of tumor rejection. IL?2 gene?transfected RenCa (RenCa/IL?2Hi) exhibited marked retardation of tumor growth when implanted in a syngeneic host. Growth retardation of RenCa/IL?2Hi was also observed in athymic nude mice even after depletion of natural killer (NK) cells by treatment with anti?asialo GM1 antibody. Histological analysis of RenCa/IL?2Hi tumors disclosed non?specific inflammatory changes in syngeneic hosts. Co?injection of Bacillus Calmette Guerin with RenCa/IL?2Hi considerably enhanced the anti?tumor effects. Taken together, these findings strongly suggest that in situ IL?2 production leads to tumor rejection through non?specific inflammatory responses without participation of T cells and NK cells. On the other hand, the syngeneic mice that had rejected RenCa/IL?2Hi acquired immunity against parental RenCa, suggesting possible participation of memory T cells in the second rejection of the tumor.
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