Abstract：
Evolutionary theory predicts that the accumulation of deleterious mutations in asexually reproducing organisms should lead to genomic decay. Clonally reproducing cell lines, i.e., transmissible cancers, when cells are transmitted as allografts/xenografts, break these rules and survive for centuries and millennia. The currently known 11 transmissible cancer lineages occur in dogs (canine venereal tumour disease), in Tasmanian devils (devil facial tumor diseases, DFT1 and DFT2), and in bivalves (bivalve transmissible neoplasia). Despite the mutation loads of these cell lines being much higher than observed in human cancers, they have not been eliminated in space and time. Here, we provide potential explanations for how these fascinating cell lines may have overcome the fitness decline due to the progressive accumulation of deleterious mutations and propose that the high mutation load may carry an indirect positive fitness outcome. We offer ideas on how these host-pathogen systems could be used to answer outstanding questions in evolutionary biology. The recent studies on the evolution of these clonal pathogens reveal key mechanistic insight into transmissible cancer genomes, information that is essential for future studies investigating how these contagious cancer cell lines can repeatedly evade immune recognition, evolve, and survive in the landscape of highly diverse hosts.
摘要：
进化理论预测，无性繁殖生物体中有害突变的积累应导致基因组衰变。克隆繁殖细胞系，即，传染性癌症,当细胞作为同种异体移植物/异种移植物传播时，打破这些规则,生存了几个世纪和几千年。目前已知的11种传染性癌症谱系发生在狗中（犬类性病，CTVT),塔斯马尼亚恶魔（魔鬼面部肿瘤疾病，DFT1和DFT2)和双壳类(双壳类传染性肿瘤，BTN）。尽管这些细胞系的突变负荷比人类癌症中观察到的高得多，他们没有在空间和时间上被淘汰。在这里，我们提供了潜在的解释，这些迷人的细胞系可能克服了由于有害突变的逐渐积累而导致的适应性下降，并提出高突变负荷可能带来间接的积极适应性结果。我们提供了有关如何使用这些宿主病原体系统来回答进化生物学中悬而未决的问题的想法。最近对这些克隆病原体进化的研究揭示了对传染性癌症基因组的关键机制。对于未来研究这些传染性癌细胞系如何反复逃避免疫识别至关重要的信息，进化，并在高度多样化的寄主景观中生存。
