Review demonstrates the mutator phenotype hypothesis in human tumors, indicating that accelerated mutation rates drive tumor heterogeneity and inform strategies for cancer prognosis and therapy.
Most human tumors are highly heterogenous. We have hypothesized that this heterogeneity results from a mutator phenotype. Our premise is that normal mutation rates are insufficient to account for the multiple mutations found in human cancers, and, instead, that cancers must exhibit a mutator phenotype early during their evolution. Here, we examine the current status and implications of the mutator phenotype hypothesis for the prognosis, treatment, and prevention of human cancers.
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Loeb et al. (2003) studied this question.
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