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本文考虑一种用肿瘤学上的病毒和抑制剂来治疗癌症的组合治疗方法.具复制能力的基因改变的腺病毒感染癌细胞,在其中复制再生并最终弓I起感染的癌细胞死亡(溶解).一旦感染的癌细胞死亡,其中的病毒释放并接着感染其他的癌细胞.病毒能否成功进入癌细胞与Coxsackie腺病毒受体(CAR)的表达密切相关.激活有丝分裂的蛋白质激酶(即著名的MEK)抑制剂能促进CAR的表达,从而导致更多的病毒进入癌细胞.然而,MEK抑制剂也能引起短暂的G1细胞循环停止,从而抑制病毒的复制再生.为了设计一个有效的治疗方案,在病毒感染的促进与病毒复制的抑制之间必须取得一个最优平衡.我们用一个数学模型来刻画病毒和抑制剂对癌细胞的影响,并用该模型来探讨:如何用上述组合治疗方法来促使肿瘤体积减少.进一步,对一定的初始细胞密度,我们发现了一个最优的抑制剂剂量.另外,最优的抑制剂实施时间也被数值地研究.
Here we consider a combination therapy that uses oncological viruses and inhibitors to treat cancer.Adenoviral replication-competent adenovirus infects cancer cells in which the cancerous cells that have undergone replication and ultimately bow-I infection die ) Once the infected cancer cells have died, the virus releases and subsequently infect other cancer cells.The successful entry of the virus into cancer cells is closely linked to the expression of the Coxsackie Adenovirus Receptor (CAR), which activates mitotic protein kinases MEK) inhibitors can promote the expression of CAR, resulting in more viruses entering the cancer cells However, MEK inhibitors can also cause short-term G1 cell cycle arrest, thereby inhibiting the replication of the virus in order to design an effective treatment , There must be an optimal balance between the promotion of viral infection and the inhibition of viral replication.We used a mathematical model to characterize the effects of viruses and inhibitors on cancer cells and used the model to explore how to use the combination therapy described above To promote tumor volume reduction.Furthermore, for a certain initial cell density, we found an optimal dose of inhibitor.In addition, the most Also investigated numerically inhibitors implementation time.