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W2047055248 abstract "have been made in our understanding of the mechanisms of host defense against cancer. More importantly, there is now evidence that, with appropriate manipulations, lymphoid effector cells can mediate the lysis of virtually all types of tumor targets, including fresh tumor cells (Grimm et al, JExp Med 1982,157B84-897). In addition, animal experiments (Mazumder and Rosenberg, J Exp Med 1984,159495-507; Shu and Rosenberg, Cancer Res 1985,45:1657-X%2) and clinical trials (Rosenberg et al., N En@ J Med 1987,316$388-897; West et a& N Engl J Med 1987,316:89FIO5) have both shown that effector cells generated in vitro [e.g. interleukin (IL)-2activated lymphocytes] can cause cancer regression when tmnsferred, in combination with IL-~, into a syngeneic turnorbearing host. Given the demonstration that e&ient host responses against tumors are mediated primarily by cellular mechanisms [either specific or non-major histocompatibility complex @R-K)-restricted], it is clear that the major advances in cancer immunotherapy will come from work in the following key areas:" @default.
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W2047055248 title "Immunotherapy and immunity to cancer: cellular mechanisms" @default.
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