Cancer in a host induces responses that increases the ability of the microenvironment to sustain the growing mass e.g. angiogenesis, but cancer cells can have varying sensitivities to these sustainability signals. Here we show that these sensitivities are significant determinants of ultimate tumor fate, especially in response to treatments and immune interactions. We present a mathematical model of cancer-immune interactions that modifies generalized logistic growth with both immune-predation and immune-recruitment. The role of a growing environmental carrying capacity is discussed as a possible regulatory mechanism for tumor growth, and this regulation is shown to modify cancer-immune interactions and the possibility of achieving immune-induced tumor dormancy. This mathematical model qualitatively matches experimental observations of immune-induced tumor dormancy as it predicts dormancy as a transient period of growth that necessarily ends in either tumor elimination or tumor escape. Since dormant tumors may exist asymptomatically and may be easier to treat with conventional therapy, understanding the mechanisms behind tumor dormancy may lead to new treatments aimed at prolonging the dormant state or converting an aggressive cancer to the dormant state.Major FindingsWe demonstrate, using a mathematical model, how the sensitivity of tumor cells to immune-mediated environmental signals can significantly alter tumor dynamics and thus treatment outcomes. Moreover, immune-induced tumor dormancy is predicted to be a transient period of tumor growth that must necessarily end in either tumor elimination or tumor escape, in agreement with several experimental observations.
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