A tumor is rarely fatal until becoming metastatic. Recent discoveries suggest that epithelial mesenchymal transition(EMT) is an important process which contributes to not only cancer metastasis but also increased stemness. Cancer cells with stem cell characteristics are called cancer stem cells (CSCs). We review recent efforts to quantify and delineate the relationship among EMT, CSC and tumor development. When the gene regulatory network is tightly regulated through the effectively fast regulatory binding, Cancer, Premalignant, Normal, CSC, stem cell (SC), Lesion and Hyperplasia states emerged. The corresponding landscape topography for all of these states can be quantified to a global way for uncovering the relationship among the tumor, metastasis, and development. On the other hand, phenotypic and functional heterogeneity is regarded as one of the greatest challenge in cancer treatment. Cancer and CSCs are heterogeneous and give rise to tumorigenic and non-tumorigenic cells during self-renewal, differentiation and epigenetic diversification. Further, if the gene regulatory network is weakly regulated through the effective slow regulatory binding (by DNA methylation or histone modification etc), multiple meta-stable states can emerge. This model can provide an epigenetic and physical rather than genetic and fixed origin of heterogeneity. Elucidating the origin of and dynamic nature of tumor cells will likely help better understand the cellular basis of therapeutic response, resistance, and relapse.

中文翻译：

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肿瘤，EMT和发育的景观观点。

肿瘤在转移之前很少致命。最近的发现表明，上皮间质转化（EMT）是一个重要的过程，不仅导致癌症转移，而且还增加了干度。具有干细胞特征的癌细胞称为癌症干细胞（CSC）。我们审查了最近的工作，以量化和描绘EMT，CSC和肿瘤发展之间的关系。当基因调控网络通过有效快速的调控结合被严格调控时，癌症，癌变前，正常，CSC，干细胞（SC），病变和增生状态就出现了。所有这些状态的相应景观地形都可以量化为一种整体方法，以揭示肿瘤，转移与发展之间的关系。另一方面，表型和功能异质性被认为是癌症治疗中的最大挑战之一。癌症和CSC是异质的，在自我更新，分化和表观遗传多样化过程中会产生致瘤和非致瘤细胞。此外，如果基因调控网络通过有效的缓慢调控结合（通过DNA甲基化或组蛋白修饰等）受到弱调控，则可能出现多个亚稳态。该模型可以提供表观遗传和物理而非遗传和固定的异质性起源。阐明肿瘤细胞的起源和动态性质将可能有助于更好地了解治疗反应，耐药性和复发的细胞基础。癌症和CSC是异质的，在自我更新，分化和表观遗传的多样化过程中会产生致瘤和非致瘤细胞。此外，如果基因调控网络通过有效的缓慢调控结合（通过DNA甲基化或组蛋白修饰等）受到弱调控，则可能出现多个亚稳态。该模型可以提供表观遗传和物理而非遗传和固定的异质性起源。阐明肿瘤细胞的起源和动态性质将可能有助于更好地了解治疗反应，耐药性和复发的细胞基础。癌症和CSC是异质的，在自我更新，分化和表观遗传的多样化过程中会产生致瘤和非致瘤细胞。此外，如果基因调控网络通过有效的缓慢调控结合（通过DNA甲基化或组蛋白修饰等）受到弱调控，则可能出现多个亚稳态。该模型可以提供表观遗传和物理而非遗传和固定的异质性起源。阐明肿瘤细胞的起源和动态性质将可能有助于更好地了解治疗反应，耐药性和复发的细胞基础。可能会出现多个亚稳态。该模型可以提供表观遗传和物理而非遗传和固定的异质性起源。阐明肿瘤细胞的起源和动态性质将可能有助于更好地了解治疗反应，耐药性和复发的细胞基础。可能会出现多个亚稳态。该模型可以提供表观遗传和物理而非遗传和固定的异质性起源。阐明肿瘤细胞的起源和动态性质将可能有助于更好地了解治疗反应，耐药性和复发的细胞基础。