Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness.
作者： Steven A. Roberts , Dmitry A. Gordenin
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摘要: The gain of a selective advantage in cancer as well the establishment complex traits during evolution require multiple genetic alterations, but how these mutations accumulate over time is currently unclear. There increasing evidence that mutator phenotype perpetuates development many human cancers. While some cases increased mutation rate result disruption DNA repair and replication or environmental exposures, other suggests endogenous damage induced by AID/APOBEC cytidine deaminases can transient localized hypermutation generating simultaneous, closely spaced (i.e. "clustered") mutations. Here, we discuss mechanisms lead to cluster formation, biological consequences their formation suggesting APOBEC mutagenesis also occur genome-wide. This raises possibility dysregulation enzymes may enable rapid malignant transformation rates without loss fitness associated with permanent mutators.
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