Modeling the effect of soluble fibrin on the immune-tumor interaction

Cancer is the second leading cause of death in the United States. It is believed that many people develop cancers in their lifetime but the immune system kills these cells without the need for outside treatments. In cancer progression, however, tumor cells may evade the immune system by a mechanism that is not fully understood. Soluble fibrin (sFn), a marker for disseminated intravascular coagulation, may play a role in evasion by tumor cells. As sFn becomes the predominant substance of the matrix surrounding the tumor cells it becomes immunosuppressive. This change from a predominantly collagen matrix to a sFn matrix could play a major role in tumor evasion. Previous research has shown that when sFn is present during the immune-tumor interaction monocyte receptors (MAC-1 and LFA-1) that, interact with CD54 on the tumor cell are altered. When sFn is bound to CD54 the LFA-1 receptor can no longer bind to the tumor cell, however, MAC-1 is still functional. If sFn binds to both, MAC-1 and CD54, then the monocyte is no longer functional against the tumor cell. A mathematical model was developed using a series of scenarios to create a set of continuous ordinary differential equations. These equations were coded in MATLAB to obtain simulations. Parameters were altered to show that the equations validated the experimental research previously published.