Abstract
Cancer dormancy is a well-recognized clinical phenomenon in which tumor cells are present, but the tumor burden does not increase for long periods of time1–3. However, tumor cells can regrow many years later. In breast cancer, there is a steady rate of recurrence 10 to 20 years after removal of the primary tumorl3,4 and the recurrent tumor frequently grows at a rapid rate(5). A particularly pertinent example is the low grade (follicular) form of non-Hodgkin’s lymphoma (NHL) in which long-term remissions are common but, eventually, virtually all die of a recurrence. Levy and Miller(5) have treated such patients with monoclonal anti-idiotype (Id) and have achieved remissions in a high proportion of patients. Relapses, many caused by Id-negative variants, are frequent indicating that the antibody (Ab) was particularly effective in inducing dormancy in cells bearing the corresponding idiotope but that hypermutation of VH and VL genes eventually allow some tumor cells from the original clone to escape(5–7).
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Uhr, J.W. et al. (1996). Role of Antibody Signaling in Inducing Tumor Dormancy. In: Gupta, S., Cohen, J.J. (eds) Mechanisms of Lymphocyte Activation and Immune Regulation VI. Advances in Experimental Medicine and Biology, vol 406. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0274-0_7
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