Bussey Kimberly J, Davies Paul C W
Precision Medicine, Midwestern University, Glendale, AZ, USA; The BEYOND Center for Fundamental Concepts in Science, Department of Physics, Arizona State University, Tempe, AZ, USA.
The BEYOND Center for Fundamental Concepts in Science, Department of Physics, Arizona State University, Tempe, AZ, USA.
Prog Biophys Mol Biol. 2021 Oct;165:49-55. doi: 10.1016/j.pbiomolbio.2021.08.002. Epub 2021 Aug 8.
Cancer or cancer-like phenomena pervade multicellular life, implying deep evolutionary roots. Many of the hallmarks of cancer recapitulate unicellular modalities, suggesting that cancer initiation and progression represent a systematic reversion to simpler ancestral phenotypes in response to a stress or insult. This so-called atavism theory may be tested using phylostratigraphy, which can be used to assign ages to genes. Several research groups have confirmed that cancer cells tend to over-express evolutionary older genes, and rewire the architecture linking unicellular and multicellular gene networks. In addition, some of the elevated mutation rate - a well-known hallmark of cancer - is actually self-inflicted, driven by genes found to be homologs of the ancient SOS genes activated in stressed bacteria, and employed to evolve biological workarounds. These findings have obvious implications for therapy.
癌症或类似癌症的现象在多细胞生物中普遍存在，这意味着其有着深厚的进化根源。癌症的许多特征重现了单细胞模式，这表明癌症的发生和发展代表了一种对压力或损伤的系统性逆转，回归到更简单的祖先表型。这种所谓的返祖理论可以通过系统发育地层学来检验，该方法可用于给基因确定年代。几个研究小组已经证实，癌细胞倾向于过度表达进化上更古老的基因，并重新连接单细胞和多细胞基因网络的架构。此外，一些升高的突变率——癌症的一个众所周知的特征——实际上是自我造成的，由那些被发现是在受应激细菌中被激活的古老SOS基因的同源基因驱动，并被用于进化出生物学上的变通方法。这些发现对治疗有着明显的启示。
