Dingli David, Traulsen Arne, Pacheco Jorge M
Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts 02138, USA.
Cell Cycle. 2007 Feb 15;6(4):461-6. doi: 10.4161/cc.6.4.3853. Epub 2007 Feb 17.
Many tumors derive from the transformation of normal stem cells into cancer stem cells that retain their self-renewal capacity. This modern view of cancer has provided a natural explanation for the striking parallels which exist between these two different types of self-renewing cells. Here we develop a simple mathematical model to investigate the implications of this concept regarding the evolution of tumors in the hematopoietic system. Our results unequivocally demonstrate that stochastic effects related to the finite size of the active stem cell population have a profound influence on the dynamics of cancer evolution. For input parameters compatible with both the natural history of human cancer and mouse models, our results show how stochastic dynamics alone may lead to both remission in some cases and rapid expansion in others.
许多肿瘤源于正常干细胞向保留自我更新能力的癌症干细胞的转变。这种现代癌症观点为这两种不同类型的自我更新细胞之间存在的显著相似之处提供了自然解释。在此，我们开发了一个简单的数学模型来研究这一概念对造血系统中肿瘤演化的影响。我们的结果明确表明，与活性干细胞群体有限大小相关的随机效应，对癌症演化动态有着深远影响。对于与人类癌症自然史和小鼠模型均兼容的输入参数，我们的结果显示了仅随机动态如何在某些情况下导致缓解，而在其他情况下导致快速扩张。
