ABSTRACT
The phenomenon of tumour dormancy has been inferred from variety of experimental and clinical observations, and in many instances some form of host control, rather than intrinsic tumour cell properties is suggested. The chapter describes experimental models where have been able to demonstrate prolonged dormancy in solid tumours and where immune mechanisms are implicated. It includes examples where tumour growth or metastasis appears to be indifferently influenced by the immune system, but where control is exercised by other factors. In order to prove experimentally that anti-tumour immunity could control disseminated disease, and to determine which cellular and/or humoral effectors might be involved, we investigated the effects of various immunosuppressive regimes on spontaneous metastasis. The experiments described so far relate to conditions where the host was immunosuppressed prior to-or concommitant with-local tumour transplantation. These procedures may have augmented metastasis by allowing increased dissemination of cells from primary site, or by enhancing the probability of survival of circulating or secondarily seeded cells.
