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.