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Numerous studies suggest that a low immune response might be beneficial, if not necessary, for tumor growth, and only a strong immune response can counter tumor growth and thus inhibit progression. Without an immune response, a heterogeneous tumor population comprised of cancer stem cells and non-stem progenitors grows as conglomerates of self-metastases [ Enderling et al. This morphological phenomenon results from the interplay of cell proliferation, cell migration and cell death. With increasing cell death intra-tumoral spatial inhibitions are loosened, which in turn enable cancer stem cell cycling and thus, counter-intuitively, tumor progression [ Enderling et al.

By overlaying on this model the diffusion of immune reactants into the tumor from a peripheral source to target cells, we simulate the process of immune-system-induced cell kill on tumor progression. A low cytotoxic immune reaction continuously kills cancer cells and, although at a low rate, thereby causes the liberation of space-constrained cancer stem cells to drive self-metastatic progression and continued tumor growth. With increasing immune system strength, however, tumor growth peaks, and then eventually falls below the intrinsic tumor sizes observed without an immune response.

Focusing only on the cytotoxic function of the immune system, we were able to observe all immunoediting roles of the immune system: immune promotion at weak immune responses, immunoinhibition at strong immune responses, and immunoselection at all levels. Simulations of our model support a hypothesis previously put forward by Prehn [ Prehn, ] that comparable tumor sizes can be observed for weak and strong immune reactions.

With this increasing immune response the number and proportion of cancer stem cells monotonically increases, implicating an additional unexpected consequence, that of cancer stem cell selection, to the immune response. We propose more generally that a stem-cell-expansive influence may take the form of anything that encourages morphological fingering. Beyond immune response, this could include cell death, or even growth within restricted thin channels, as might be expected e. Tumor-host signaling interaction reveals a systemic, age-dependent splenic immune influence on tumor development.

Proton irradiation impacts age-driven modulations of cancer progression influenced by immune system transcriptome modifications from splenic tissue. J Radiat Res.

Quantitative Modeling and Simulations

Epub Aug 7. In: d'Onofrio A, Gandolfi A eds. Mathematical Oncology Wilkie KP , Hahnfeldt P. Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion. Interface Focus. Epub Jun J Hematol Oncol. Tumor—immune dynamics regulated in the microenvironment inform the transient nature of immune-induced tumor dormancy. Cancer Res. Further, the Stephen Hart.

Microenvironment of tumours key to cancer's progression

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