<p>We propose a mathematical model for the growth and treatment of Undifferentiated Pleomorphic Sarcoma (UPS) using a system of nonlinear differential equations. The model combines Gompertz-type tumor growth with surface-dependent necrotic loss, surgical resection with residual disease, postoperative recovery, tumor–immune interaction, and radiation treatment scheduling. We study the mathematical properties of the model and obtain several results. The growth equation shows the existence of a threshold below which the tumor cannot survive and may disappear. The postoperative phase exhibits an early inflammatory stage followed by proliferative recovery. For the tumor-immune subsystem, equilibrium states and local stability conditions are identified. The radiation treatment problem is formulated as an optimal control problem, and the optimal strategy is shown to be of bang-bang type. The model suggests that tumor recurrence depends not only on tumor growth itself but also on residual disease, postoperative dynamics, immune response, and treatment timing.</p>

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A Mathematical Model to Predict Growth and Treatment for UPS Cancer

  • Sumit Roy

摘要

We propose a mathematical model for the growth and treatment of Undifferentiated Pleomorphic Sarcoma (UPS) using a system of nonlinear differential equations. The model combines Gompertz-type tumor growth with surface-dependent necrotic loss, surgical resection with residual disease, postoperative recovery, tumor–immune interaction, and radiation treatment scheduling. We study the mathematical properties of the model and obtain several results. The growth equation shows the existence of a threshold below which the tumor cannot survive and may disappear. The postoperative phase exhibits an early inflammatory stage followed by proliferative recovery. For the tumor-immune subsystem, equilibrium states and local stability conditions are identified. The radiation treatment problem is formulated as an optimal control problem, and the optimal strategy is shown to be of bang-bang type. The model suggests that tumor recurrence depends not only on tumor growth itself but also on residual disease, postoperative dynamics, immune response, and treatment timing.