Somatic mutations in oncogene and tumor suppressor genes accumulate in healthy tissues throughout life and delineate clones with limited expansion. Lifestyle‐related toxic insults increase the size and number of these clones that participate to tissue aging. Their identification has blurred the boundaries between clonal expansion and malignant tumor and has drawn more attention to the role of the host environment in tumor emergence and progression. Local tissue factors such as disrupted cell interactions and stromal cell senescence combine with systemic and distant alterations to initiate the reiterative process of clonal expansion, multilayer intrinsic diversification and clonal selection that eventually characterize overt tumor evolution. In turn, tumors remodel their close and distant environments, establishing positive feedback loops that contribute to disease progression. Strategies emerge to preserve the tumor suppressive properties of healthy tissue landscapes and delay age‐induced changes that eventually lead to cancer.

中文翻译：

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宿主环境在癌症进化中的作用

癌基因和肿瘤抑制基因的体细胞突变在整个生命周期中都在健康组织中积累，并描述了有限扩展的克隆。与生活方式有关的有毒侮辱增加了参与组织衰老的这些克隆的大小和数量。他们的鉴定模糊了克隆扩增和恶性肿瘤之间的界限，并引起了人们对宿主环境在肿瘤发生和发展中的作用的更多关注。局部组织因子（如破坏的细胞相互作用和基质细胞衰老）与全身和远处的改变相结合，从而引发了克隆扩展，多层内在多样化和克隆选择的重复过程，最终表征了明显的肿瘤进化。反过来，肿瘤会重塑它们近距离和远处的环境，建立有助于疾病发展的积极反馈回路。可以保留健康组织景观的肿瘤抑制特性并延缓年龄诱发的变化，最终导致癌症的变化。