A mathematical model for the regulation of tumor dormancy based on enzyme kinetics
Abstract
We present a two compartment model for tumor dormancy based on an idea of Zetter to wit: The vascularization of a secondary (daughter) tumor can be suppressed by inhibitor originating from a larger primary (mother) tumor. We apply this idea at the avascular level to develop a model for the remote suppression of secondary avascular tumors via the secretion of primary avascular tumor inhibitors. The model gives good agreement with experimental observation (Derm. Surg. 29(2003) 664-667). The authors reported on the emergence of a polypoid melanoma at a site remote from a primary polypoid melanoma after excision of the latter . The authors observed no recurrence of the melanoma at the primary site, but did observe secondary tumors at secondary sites five to seven centimeters from the primary site within a period of one month after the excision of the primary site. We attempt to provide a reasonable biochemical/cell biological model for this phenomenon. We show that when the tumors are sufficiently remote, the primary tumor will not influence the secondary tumor while, if they are too close together, the primary tumor can effectively prevent the growth of the secondary tumor, even after it is removed. It should be possible to use the model as the basis for a testable hypothesis which could be checked in a controlled in vitro experiment.
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