The cancer stem cell hypothesis claims that tumor growth and progression are driven by a (typically) small niche of the total cancer cell population called cancer stem cells (CSCs). These CSCs can go through symmetric or asymmetric divisions to differentiate into specialised, progenitor cells or reproduce new CSCs. While it was once held that this differentiation pathway was unidirectional, recent research has demonstrated that differentiated cells are more plastic than initially considered. In particular, differentiated cells can de-differentiate and recover their stem-like capacity. Two recent papers have considered how this rate of plasticity affects the evolutionary dynamic of an invasive, malignant population of stem cells and differentiated cells into existing tissue (Mahdipour-Shirayeh et al., 2017; Wodarz, 2018). These papers arrive at seemingly opposing conclusions, one claiming that increased plasticity results in increased invasive potential, and the other that increased plasticity decreases invasive potential. Here, we show that what is most important, when determining the effect on invasive potential, is how one distributes this increased plasticity between the compartments of resident and mutant-type cells. We also demonstrate how these results vary, producing non-monotone fixation probability curves, as inter-compartmental plasticity changes when differentiated cell compartments are allowed to continue proliferating, highlighting a fundamental difference between the two models. We conclude by demonstrating the stability of these qualitative results over various parameter ranges. Keywords: cancer stem cells, plasticity, de-differentiation, fixation probability.

癌症干细胞假说声称肿瘤生长和进展是由（通常）总癌细胞群中的一个小生态位驱动的，称为癌症干细胞 (CSC)。这些 CSC 可以通过对称或不对称分裂分化成专门的祖细胞或复制新的 CSC。虽然曾经认为这种分化途径是单向的，但最近的研究表明，分化的细胞比最初认为的更具可塑性。特别是，分化的细胞可以去分化并恢复其干细胞样能力。最近的两篇论文考虑了这种可塑性如何影响侵入性恶性干细胞群和分化细胞进入现有组织的进化动态（Mahdipour-Shirayeh 等人，2017 年；Wodarz，2018 年）。这些论文得出了看似相反的结论，一篇声称可塑性增加会导致侵入潜力增加，而另一篇则声称可塑性增加会降低侵入潜力。在这里，我们表明，在确定对侵入潜力的影响时，最重要的是如何在常驻细胞和突变型细胞的隔间之间分配这种增加的可塑性。我们还展示了这些结果如何变化，产生非单调固定概率曲线，因为当允许分化的细胞室继续增殖时，室间可塑性发生变化，突出了两种模型之间的根本差异。最后，我们证明了这些定性结果在各种参数范围内的稳定性。关键词：癌症干细胞，可塑性，去分化，