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Strategy for treating MUC1-expressing tumors depends upon tumor origin.
2002 OCT 16 - (NewsRx.com & NewsRx.net) -- by Maria G. Essig, MS, ELS, senior medical writer - MUC1-expressing tumors that originate in different organs require different effector cells and mechanistic tactics for elimination, according to a report in Cancer Immunology Immunotherapy.
"In this study, we characterized molecular components that are required to produce immune responses that eliminate Panc02.MUC1 tumors in vivo by utilizing mice genetically deficient in molecules related to immunity," reported Connie L. Sivinski and colleagues at the University of Nebraska Medical Center in Omaha.
The investigators found that CD8+ effector cells were necessary to destroy Panc02 tumors that expressed MUC1. The elimination of MUC1-expressing Panc02 tumors also depended upon the actions of T cells that expressed T-cell receptor-alpha/beta (TCR-alpha/beta) and on CD28 and CD40:CD40L interactions.
Of the type 1 cytokines, interferon-gamma (IFN-gamma) was needed to eradicate MUC1-expressing Panc02 tumors. In contrast, neither of the type 2 cytokines interleukin-4 (IL-4) or interleukin-10 (IL-10) played a role in tumor rejection (Molecular requirements for CD8-mediated rejection of a MUC1-expressing pancreatic carcinoma: implications for tumor vaccines. Cancer Immunol Immunother, 2002;51(6):327-340).
Major histocompatibility complex (MHC) class I molecules on Panc02.MUC1 tumor cells could be upregulated by IFN-gamma, but MHC class II molecules could not. Protection against Panc02.MUC1 tumors required lymphotoxin-alpha but not tumor necrosis factor receptor 1 (TNFR-1).
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Source: HighBeam Research, Strategy for treating MUC1-expressing tumors depends upon tumor...