Tumor-Host Interaction

Reaction-diffusion models have very successfully accounted for the interaction between normal and tumor cells. The diffusion terms in these models can be broadly divided into two categories, linear and nonlinear diffusion. In linear diffusion models, the flux of one cell type depends only on the concentration of cells of the same type. In nonlinear diffusion models, the presence of one cell type affects the diffusion of cells of a different type. Models with nonlinear diffusion have described the spatial dispersal and temporal development of tumor tissue, normal tissue, and excess H ion concentration [155]. They assume that transformation-induced reversion of neoplastic tissue creates a microenvironment around the tumor where tumor cells survive and proliferate, whereas normal cells do not remain viable. These conditions, favorable for tumor cells and unfavorable for normal cells, are due to 

Mendez et al., Reaction-Transport Systems, Springer Series in Synergetics, DOI 10.1007/978-3-642-11443-4 8, Springer-Verlag Berlin Heidelberg 2010 

We assumed Lotka-Volterra kinetics between tumor and normal cells in (8.1). The maximum growth rates of normal and tumor cells, i.e., the net result of tumor cell doubling minus tumor cells loss from apoptosis or necrosis, are and r.  

State I is the trivial solution it is unstable and biologically irrelevant. State II corresponds to normal, healthy tissue without tumor cells. The system evolves to this state, regardless of the initial state, if bf jKj and bjf Kf K-j-. If the initial state is sufficiently close to State n, only the second condition needs to be satisfied. State III corresponds to complete tumor invasion with total destruction of normal tissue. The system evolves to this state, regardless of the initial state, if bNT T mdbju/Knj A j. Ifthe initial state is sufficiently close to State III, only the first condition is needed. State rv corresponds to a state of coexistence between tumor and normal cells. The system evolves to this state, if bf jKj Kn 

In this model, an invasive cancer, where the tumor edge advances as a propagating front into normal tissue, corresponds to a transition to a stable state containing tumor cells, state III or IV. The Hamilton-Jacobi formalism provides the propagation velocity of a front connecting state II to state HI, an invasive tumor front. 

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T-Lymphocytes (4,5) and other cellular components of the immune system also have equally wide implications in regulation of the normal immune system. The T-lymphocytes play a central role in the body s response to harmful antigens and tumor—host interaction (4). Responses involve antigens derived from vimses, bacteria, parasites, and tumors. T-ceUs also participate in the immune surveillance response, where self-antigens are recognized, but usually sequestered within the cell and, when exposed, become markers of cellular damage. 

Bl. Baici, A., Gyger-Marazzi, M., and Strauli, P., Extracellular cysteine proteinase and col-lagenase activities as a consequence of tumor-host interaction in the rabbit V2 carcinoma. Invasion Metastasis 4, 13-27 (1984). 

Pluen, A., Boucher, Y., Ramanujan, S., McKee, T.D., Gohongi, T., di Tomaso, E. et al. (2001) Role of tumor-host interactions in interstitial diffusion of macromolecules Cranial Verses subcutaneous tumors. Proc. Natl. Acad. Sci. USA, 98, 4628 1633. 

Sugarbaker, E. V. (1979). Cancer metastasis a product of tumor-host interactions. Curr. Probl. Cancer 3, 1-59. 

IL-2 and IL-15, which uses the (3- and y-chains of the IL-2R, have been found in melanoma cells and anti-IL-15 mAbs to inhibit HLA class I expression in these cells. Therefore these cytokines may modify the behavior of both stromal and neoplastic cells inside a tumor. These data may have important implications for our understanding of tumor-host interactions and in future strategies of immunotherapy. When compared with lL-2, which enhances both spontaneous and antigen-induced lymphocyte proliferative responses, IL-15 rarely increases spontaneous lymphocyte proliferation. Thus IL-15 may help to correct the impaired profiferative response of CD4 lymphocytes from HlV-l-infected persons without the mitogenic effect of IL-2, which also may induce HIV-1 expression. "... 

L2 Tumor-Host Interaction with Contact Inhibition... 

Obtain the velocity of the invasion front (8.6) and the recovery front (8.7) for the tumor-host interaction model given by (8.1). 

Ben-Baruch, A. (2003). Host microenvironment in breast cancer development Inflammatory cells, cytokines and chemokines in breast cancer progression Reciprocal tumor-microenvironment interactions. Breast Cancer Res. 5, 31-36. 

Chishima, T., Miyagi, Y, Li, L., Tan, Y, Baranov, E., Yang, M., Shimada, H., Moossa, A. R. and Hoffman, R. M. (1997e) Use of histoculture and green fluorescent protein to visualize tumor cell host interaction. In Vitro Cell Dev. Biol. Anim. 33, 745-747. 

Rheb, Modulation of Survival, and Host-Tumor Interactions. 144... 

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