| First Author | Blankenstein T | Year | 2003 |
| Journal | Adv Cancer Res | Volume | 90 |
| Pages | 179-207 | PubMed ID | 14710951 |
| Mgi Jnum | J:88116 | Mgi Id | MGI:3029136 |
| Doi | 10.1016/s0065-230x(03)90006-6 | Citation | Blankenstein T, et al. (2003) Chemical carcinogens as foreign bodies and some pitfalls regarding cancer immune surveillance. Adv Cancer Res 90:179-207 |
| abstractText | Interferon-gamma-receptor (IFN-gammaR)-deficient mice are more susceptible to tumor induction by methylcholanthrene (MCA) in comparison to control littermates. The cellular source of IFNgamma is not known, but the absence of T cells does not significantly increase the incidence of MCA-induced tumors. However, it appears that the presence of T cells in combination with unknown, perhaps environmental, factors can decrease MCA-induced tumor incidence, indicating that IFN-gamma of unknown origin contributes to the protective response. The current knowledge of cancer biology, immune regulation, and tumor-promoting effects of inflammation are difficult to reconcile with the concept of immune surveillance against non-virus-associated cancer. Analysis of the primary MCA-treated mouse indicates, as one protective mechanism, a tissue repair response against MCA-induced damage, in the course of which MCA is encapsulated and persists for long time in tumor-free mice, termed foreign-body reaction. The protection from DNA damage could simultaneously diminish tissue injury and malignant transformation. We argue that inhibition of MCA-induced carcinogenesis is mechanistically different from tumor transplantation immunity and that a longer latency in MCA-treated mice is unlikely due to T cell-mediated tumor recognition and selection of less immunogenic variants. We discuss that the IFNgammaR-dependent mechanism against MCA is unrelated to the original concept of T cell-mediated immune surveillance and that the increased spontaneous tumor incidence observed in some immune-deficient mice is likely to be explained by opportunistic infection and tumor-promoting chronic inflammation. |
