We established a model of orthotopic injection of a syngeneic pancreatic tumor cell line in C57BL/6 mice and evaluated the effects of organ site on induction of immunity to a
tumor-specific
antigen, MUC1. Mice were challenged with a syngeneic pancreatic
adenocarcinoma cell line that expressed MUC1 (Panc02-MUC1) by orthotopic injection into the pancreas, or by
subcutaneous injection.
Tumor cells injected into the pancreas grew much faster than those injected subcutaneously. Mice challenged subcutaneously with Panc02-MUC1 rejected
tumors or developed slowly growing
tumors that were negative for MUC1 expression. In contrast, mice challenged orthotopically into the pancreas developed progressive
tumors that were positive for MUC1 expression. Sera from mice that rejected PancO2-MUC1 (
tumor-immune mice) showed no detectable
IgG1 and
IgM titers against the
MUC1 tandem-repeat peptide, whereas mice with progressive
tumor growth had significant titers of
IgG1 and
IgM specific for MUC1. This suggests that the humoral immune response was ineffective in mediating
tumor rejection. The results show that the growth properties and immunological rejection of pancreatic
tumors is affected by the organ site at which the
tumor grows.