Feunteun Jean, Ostyn Pauline, Delaloge Suzette
INSERM U981, Gustave Roussy, Université Paris-Saclay, Villejuif, France.
UMR 9019, Gustave Roussy, Université Paris-Saclay, Villejuif, France.
iScience. 2022 Apr 8;25(5):104217. doi: 10.1016/j.isci.2022.104217. eCollection 2022 May 20.
Since the discovery of oncogenes and tumor suppressor genes in the late past century, cancer research has been overwhelmingly focused on the genetics and biology of tumor cells and hence has addressed mostly cell-autonomous processes with emphasis on traditional driver/passenger genetic models. Nevertheless, over that same period, multiple seminal observations have accumulated highlighting the role of non-cell autonomous effectors in tumor growth and metastasis. However, given that cell autonomous and non-autonomous events are observed together at the time of diagnosis, it is in fact impossible to know whether the malignant transformation is initiated by cell autonomous oncogenic events or by non-cell autonomous conditions generated by alterations of the tissue-body ecosystem. This review aims at addressing this issue by taking the option of defining malignancy as a complex genetic trait incorporating genetically determined reciprocal interactions between tumor cells and tissue-body ecosystem.
自上世纪末发现癌基因和肿瘤抑制基因以来，癌症研究绝大多数都集中在肿瘤细胞的遗传学和生物学上，因此主要探讨的是细胞自主过程，重点是传统的驱动/乘客基因模型。然而，在同一时期，多项具有开创性的观察结果不断积累，凸显了非细胞自主效应因子在肿瘤生长和转移中的作用。然而，鉴于在诊断时细胞自主和非自主事件是同时被观察到的，实际上不可能知道恶性转化是由细胞自主致癌事件引发的，还是由组织 - 身体生态系统改变所产生的非细胞自主条件引发的。本综述旨在通过选择将恶性肿瘤定义为一种复杂的遗传特征来解决这一问题，这种遗传特征包含了肿瘤细胞与组织 - 身体生态系统之间由基因决定的相互作用。
