Metastases are the major cause of cancer patients' mortality and can occur years and even decades following apparently successful treatment of the primary tumor. Early dissemination of cancer cells, followed by a protracted period of dormancy at distant sites, has been recently recognized as the clinical explanation for this very-long latency. The mechanisms that govern tumor dormancy at distant sites and their reactivation to proliferating metastases are just beginning to be unraveled. Tumor cells, that survive the immune surveillance and hemodynamic forces along their journey in the circulation and successfully colonize and adopt to the new and "hostile" microenvironment and survive in a quiescent dormant state for years before emerging to proliferative state, must display high plasticity. Here we will discuss whether the plasticity of dormant tumor cells is required for their long-term survival and outgrowth. Specifically, we will focus on whether epithelial mesenchymal transition and acquisition of stem-like properties can dictate their quiescent and or their proliferative fate. Deeper understanding of these intertwining processes may facilitate in the future the development of novel therapies.

中文翻译：

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肿瘤休眠和过度生长中的EMT和Stemness：它们是否交织在一起？

转移是癌症患者死亡的主要原因，在原发性肿瘤治疗成功后可能发生数年甚至数十年。最近已经认识到癌细胞的早期传播，然后在遥远的位置延长休眠期，是这种非常长的潜伏期的临床解释。远处控制肿瘤休眠的机制及其对增殖转移的再激活机制才刚刚被阐明。在循环过程中幸免于免疫监视和血液动力的肿瘤细胞必须成功展现出高可塑性，该肿瘤细胞必须在新的和“敌对的”微环境中成功定殖并适应新的“敌对”微环境，并在静止的休眠状态下存活数年。在这里，我们将讨论休眠肿瘤细胞的可塑性是否是其长期生存和生长所必需的。具体来说，我们将关注于上皮间质转化和获得茎样特性是否可以决定其静止状态或增殖命运。对这些相互交织的过程的更深入的了解可能会在将来促进新型疗法的发展。