Tumors arise through waves of genetic alterations and clonal expansion that allow tumor cells to acquire cancer hallmarks, such as genome instability and immune evasion. Recent genomic analyses showed that the vast majority of cancer driver genes are mutated in a tissue-dependent manner, that is, are altered in some cancers but not others. Often the tumor type also affects the likelihood of therapy response. What is the origin of tissue specificity in cancer? Recent studies suggest that both cell-intrinsic and cell-extrinsic factors play a role. On one hand, cell type-specific wiring of the cell signaling network determines the outcome of cancer driver gene mutations. On the other hand, the tumor cells' exposure to tissue-specific microenvironments (e.g. immune cells) also contributes to shape the tissue specificity of driver genes and of therapy response. In the future, a more complete understanding of tissue specificity in cancer may inform methods to better predict and improve therapeutic outcomes.

中文翻译：

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并非所有癌症都是一样的：癌症基因和途径的组织特异性。


肿瘤是通过一波又一波的基因改变和克隆扩张而产生的，这些改变和克隆扩张使肿瘤细胞获得癌症标志，例如基因组不稳定和免疫逃避。最近的基因组分析表明，绝大多数癌症驱动基因以组织依赖性方式发生突变，也就是说，在某些癌症中发生改变，而在其他癌症中则不会。通常，肿瘤类型也会影响治疗反应的可能性。癌症组织特异性的起源是什么？最近的研究表明，细胞内在因素和细胞外在因素都发挥着作用。一方面，细胞信号网络的细胞类型特异性布线决定了癌症驱动基因突变的结果。另一方面，肿瘤细胞暴露于组织特异性微环境（例如免疫细胞）也有助于形成驱动基因和治疗反应的组织特异性。将来，对癌症组织特异性的更全面了解可能会为更好地预测和改善治疗结果的方法提供信息。