作者: AndrewJ.G. Simpson
DOI: 10.1016/S0065-230X(08)60100-1
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摘要: Publisher Summary The chapter examines what is known (and unknown) and might be deduced indirectly concerning the frequency of somatic mutations in terms understanding human carcinogenesis. Much recent attention has been paid to important role DNA mismatch repair system controlling accumulation tissues association deficiency with focuses on examination reinterpretation data instability microsatellites tumors, which are consistent normal being highly genetically variable. Subsequently, other avenues research reviewed that indicate presence frequent tissues, number increases exponentially age. likelihood high level due spontaneous events discussed, underlying rate related germline. Based these comparisons, a simple model life cycle elaborated. This proposes overall mutation rate, manifested both germline cells, fundamental biological pacemaker defines not only rhythm evolutionary change but also longevity individual members species, limited at least part by development fatal mutation-dependent pathologies such as cancer.