Tumor Progression and <i>p53</i> LOH in <i>p19^Arf /p53</i> Compound Mutant Mice

<div><p>(A) Average number of carcinomas per mouse is plotted against the number of weeks postinitiation. Tumor progression was accelerated in all <i>p19^Arf (Arf)-</i> and <i>p53</i>-deficient genotypes compared to wild-type littermates<i>.</i> Carcinoma latency and multiplicity was almost identical for <i>p19^Arf−/−</i> mice regardless of <i>p53</i> genotype (<i>p53^+/+, p53^+/−,</i> or <i>p53^−/−</i>).</p> <p>(B) LOH of the wild-type <i>p53</i> allele by semiquantitative PCR in <i>p19^Arf /p53</i> compound tumors. Gradient made from kidney DNA used for quantitation of wt/mu ratio (top row). wt, wild-type allele; mu, knockout allele; asterisk, tumors with reduction of wild-type <i>p53.</i></p>