one factor is how many copies of the p53 tumor suppressor gene they have. larger animals (with more cells) tend to have more copies of p53. p53 causes cells to self-destruct if they go off-script. many cancers have p53 mutations to thwart this.

iirc senescence blocks damaged (potentially pre-cancerous) cells from reproducing, but unlike p53 doesn't kill them. replacing sensescent cells means more cell divisions, which also risks a cancerous mutation. so reducing senescence probably means making p53 more sensitive and redundant.