Human cancers share properties referred to as hallmarks, among which sustained proliferation, escape from apoptosis, and genomic instability are the most pervasive. The sustained proliferation hallmark can be explained by mutations in oncogenes and tumor suppressors that regulate cell growth, whereas the escape from apoptosis hallmark can be explained by mutations in the TP53, ATM, or MDM2 genes. A model to explain the presence of the three hallmarks listed above, as well as the patterns of genomic instability observed in human cancers, proposes that the genes driving cell proliferation induce DNA replication stress, which, in turn, generates genomic instability and selects for escape from apoptosis. Here, we review the data that support this model, as well as the mechanisms by which oncogenes induce replication stress. Further, we argue that DNA replication stress should be considered as a hallmark of cancer because it likely drives cancer development and is very prevalent.

中文翻译：

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DNA复制压​​力是癌症的标志。

人类癌症具有被称为标志的特性，其中最普遍的是持续增殖，逃避凋亡和基因组不稳定。持续增殖的特征可以通过调节细胞生长的癌基因和肿瘤抑制因子的突变来解释，而逃避细胞凋亡的特征可以通过TP53，ATM或MDM2基因的突变来解释。一个模型可以解释上面列出的三个特征的存在，以及在人类癌症中观察到的基因组不稳定性的模式，该模型提出，驱动细胞增殖的基因会诱导DNA复制压​​力，进而产生基因组不稳定性并选择逃避从细胞凋亡。在这里，我们回顾了支持该模型的数据，以及致癌基因诱导复制压力的机制。进一步，