Abstract
It is generally accepted that the spontanous generation of cancer cells is a common event and that the immune system ensures strict surveillance with the detection and elimination of these cells. In order to fight cancer, the idea of using the destructive power of immunologic reactions is easily visualized in autoimmune diseases and by the rejection of allografts in transplantation medicine. A number of clinical observations in human malignant melanoma suggest that a particularly vigorous immune response occurs [18,28,29,31]. It is believed that the immune attack against melanoma cells may be responsible for the occurrence of spontanous melanoma regressions and for the concomittant destruction of melanocytes in benign lesions, leading to clinical phenomena such as halo nevi, uveitis, and vitiligo in melanoma patients. In addition, tumor dormancy with a prolonged interval between the occurrence of the primary tumor and melanoma metastases has been interpreted as indicating the existence of specific, immunologic antitumor effector mechanisms. These observations, together with anecdotal and clinical reports of tumor regressions following bacterial infections or more specific immune interventions, suggest that melanoma is a good model with which to evaluate the various strategies of immune therapy [28,29,31].
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Schadendorf, D. (1997). Cytokines and Cytokine Gene Transfer in Cancer Treatment. In: Burg, G., Dummer, R.G. (eds) Strategies for Immunointerventions in Dermatology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60752-3_16
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DOI: https://doi.org/10.1007/978-3-642-60752-3_16
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