Historically, it has been widely presumed that differentiated cells are determined during development and become irreversibly committed to their designated fates. In certain circumstances, however, differentiated cells can display plasticity by changing their identity, either by dedifferentiation to a progenitor-like state or by transdifferentiation to an alternative differentiated cell type. Such cellular plasticity can be triggered by physiological or oncogenic stress, or it can be experimentally induced through cellular reprogramming. Notably, physiological stresses that promote plasticity, such as severe tissue damage, inflammation, or senescence, also represent hallmarks of cancer. Furthermore, key drivers of cellular plasticity include major oncogenic and tumor suppressor pathways and can be exacerbated by drug treatment. Thus, plasticity may help cancer cells evade detection and treatment. We propose that cancer can be considered as a disease of excess plasticity, a notion that has important implications for intervention and treatment.

中文翻译：

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癌症进展和治疗中的谱系可塑性。


从历史上看，人们普遍认为分化的细胞是在发育过程中决定的，并且不可逆转地致力于其指定的命运。然而，在某些情况下，分化细胞可以通过改变其身份来显示可塑性，或者通过去分化为祖细胞样状态，或者通过转分化为替代的分化细胞类型。这种细胞可塑性可以由生理或致癌应激触发，也可以通过细胞重编程进行实验诱导。值得注意的是，促进可塑性的生理压力，例如严重的组织损伤、炎症或衰老，也是癌症的标志。此外，细胞可塑性的关键驱动因素包括主要的致癌和肿瘤抑制途径，并且可能因药物治疗而加剧。因此，可塑性可能有助于癌细胞逃避检测和治疗。我们认为癌症可以被视为一种可塑性过度的疾病，这一概念对干预和治疗具有重要意义。