PLoS ONE：可模拟肿瘤状态的计算机模型有助癌症治疗

  千百年来，人类一直在同癌症作斗争，战斗有时候会胜利、会失败、也会处于僵持状态；在胰腺癌中，这种所谓的僵持状态就被称为肿瘤休眠，在其转变成恶性状态之前会维持长达25年，但至今尚无研究人员清楚这种机制。
  近日，一项发表在国际杂志PLoS ONE上的研究论文中，来自普林斯顿大学的研究人员开发出了一种新型的计算机模型，其可以帮助阐明休眠肿瘤周围的环境以及将肿瘤开启为恶性状态的开关，这种细胞自助模型可以模拟多种肿瘤生长、抑制、休眠及增殖的场景。
  研究者Torquato教授表示，该模型的强大之处就在于其可以帮助检测医学中现实的场景，而在未来研究中这些场景也将被用于进行实验室研究。对于每一个场景而言，都必须对虚拟的细胞群体进行设定，这些设定可能是相互作用，比如相邻细胞的死亡或者免疫系统抑制等，一旦科学家进行了规则的设定，他们就会观察到肿瘤同环境因子间的相互作用。
  文章中，研究者还评估了一系列影响肿瘤生长的因子，包括表型改变、机械性能以及抑制因子的比例和特性，研究者通过设计该计算机模型还发现，肿瘤或许在以高压及高密度为特性的环境中会被抑制。研究小组预测，如果肿瘤分裂细胞达到一定水平，那么肿瘤很有可能会快速生长，而相关结果将为开发早期癌症的治疗方法带来帮助和希望。（转化医学网360zhyx.com）

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转化医学网推荐的原文摘要：

A Cellular Automaton Model for Tumor Dormancy: Emergence of a Proliferative Switch
PLoS ONE DOI: 10.1371/journal.pone.0109934
Chen, Yang Jiao, Salvatore Torquato.
Malignant cancers that lead to fatal outcomes for patients may remain dormant for very long periods of time. Although individual mechanisms such as cellular dormancy, angiogenic dormancy and immunosurveillance have been proposed, a comprehensive understanding of cancer dormancy and the “switch” from a dormant to a proliferative state still needs to be strengthened from both a basic and clinical point of view. Computational modeling enables one to explore a variety of scenarios for possible but realistic microscopic dormancy mechanisms and their predicted outcomes. The aim of this paper is to devise such a predictive computational model of dormancy with an emergent “switch” behavior. Specifically, we generalize a previous cellular automaton (CA) model for proliferative growth of solid tumor that now incorporates a variety of cell-level tumor-host interactions and different mechanisms for tumor dormancy, for example the effects of the immune system. Our new CA rules induce a natural “competition” between the tumor and tumor suppression factors in the microenvironment. This competition either results in a “stalemate” for a period of time in which the tumor either eventually wins (spontaneously emerges) or is eradicated; or it leads to a situation in which the tumor is eradicated before such a “stalemate” could ever develop. We also predict that if the number of actively dividing cells within the proliferative rim of the tumor reaches a critical, yet low level, the dormant tumor has a high probability to resume rapid growth. Our findings may shed light on the fundamental understanding of cancer dormancy.