Analysis of Survivin’s Role in Benign and Metastasis Tumor Growth - Abstract
Purpose: In this article, we present a modified cancerous stem cell-survivin model to simulate the effect of the YM155 drug and radiation therapy as a combination treatment on the tumor growth. Radio resistant mechanism is illustrated by this model.
Methods: According to experimental studies by Iwasa (2008), the combination treatment inhibits survivin expression. Modified cancerous stem cell-survivin model simulates these experimental studies. Then, we introduce a modified stochastic differential equations model for the metastasis tumors. The tumor growth
equations of the stochastic differential equations model are not as good as cancer stem cell-survivin model. The modified stochastic differential equations model uses the cancerous stem cell-survivin model instead of tumor growth equations in the stochastic differential equations model.
Result: Here, the modified cancerous stem cell-survivin model confirms experimental studies significantly more precise than the cancerous stem cell-survivin model. Also, the modified stochastic differential equations model uses the cancerous stem cell-survivin model instead of tumor growth equations in the stochastic differential equations model.
Conclusion: The modified cancerous stem cell-survivin model reveals that survivin first regulates cell division through interaction with proteins INCENP and Aurora B; then, YM155 drug inhibits survivin. Therefore, it seems that this mechanism leads to radioresistance. The YM155 drug only reduces radio resistance, since it is not a survivin-inhibitor as quick as survivin which regulates cell division. Even the more dose of the YM155 drug will not create a perfect therapy. The velocity of a survivin-inhibition drug has an effective role in the combination treatment.