A panel of 10 digestive tract carcinoma cell lines (6 pancreatic carcinomas) was assayed for their sensitivity to HuLelFN, human rIFN-7, rTNF-a and allogeneic human LAK-cells in vitro. In addition, a combination of rlFN-7 +rTNF-a was tested on 3 pancreatic carcinoma cell lines. Whereas 6/7 cell lines were completely resistant to HuLelFN, rIFN-7 and rTNF-α did inhibit growth of some carcinomas tested. The individual sensitivity was heterogenous as is already known from cytostatics. Response to rIFN-γ tended to increase with increment of cell doubling time. Only high concentrations (>1000 U/mL) of rIFN-γ displayed cytotoxicity on sensitive tumors. The antitumoral effect of rIFN-γ was stimulated by rTNF-α. As revealed by isobole analysis this interaction was synergistic in all pancreatic carcinomas tested. In comparison to rIFN-γ or rTNF-α the response to LAK-cells was slightly superior at high effector target ratios, even though hetero
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