Pereira Lloyd, Mariadason John M, Hannan Ross D, Dhillon Amardeep S
Research Division, Peter MacCallum Cancer Centre , Melbourne, VIC , Australia.
Olivia Newton-John Cancer Research Institute, Austin Hospital , Melbourne, VIC , Australia.
Front Oncol. 2015 Feb 2;5:13. doi: 10.3389/fonc.2015.00013. eCollection 2015.
Colorectal cancer (CRC) is a genetically heterogeneous disease that develops and progresses through several distinct pathways characterized by genomic instability. In recent years, it has emerged that inherent plasticity in some populations of CRC cells can contribute to heterogeneity in differentiation state, metastatic potential, therapeutic response, and disease relapse. Such plasticity is thought to arise through interactions between aberrant signaling events, including persistent activation of the APC/β-catenin and KRAS/BRAF/ERK pathways, and the tumor microenvironment. Here, we highlight key concepts and evidence relating to the role of epithelial-mesenchymal plasticity as a driver of CRC progression and stratification of the disease into distinct molecular and clinicopathological subsets.
结直肠癌（CRC）是一种基因异质性疾病，通过以基因组不稳定为特征的几种不同途径发展和进展。近年来，已发现CRC细胞的某些群体中固有的可塑性可导致分化状态、转移潜能、治疗反应和疾病复发的异质性。这种可塑性被认为是通过异常信号事件之间的相互作用产生的，包括APC/β-连环蛋白和KRAS/BRAF/ERK途径的持续激活以及肿瘤微环境。在这里，我们强调了与上皮-间质可塑性作为CRC进展的驱动因素以及将该疾病分层为不同分子和临床病理亚组的作用相关的关键概念和证据。
