Human cancer rates vary dramatically across the range of internal organs in the body, but there is no single model to explain the variation and there is also no obvious overall pattern to it. Theories have been proposed to account for high rates in particularly cancer-prone organs, and they usually concentrate on the peculiar vulnerability of certain cells to mutation (e.g., lung cells' direct exposure to airborne carcinogens). These explanations are valuable for understanding mechanisms of disease and also for cancer prevention, but they address neither the overall distribution of cancers nor the possibility that some states of differentiation may be intrinsically less stable than others to the effects of random mutation, a possibility predicted on purely theoretical grounds many years ago. This brief report describes an overall pattern to human organ-specific cancer incidence data and shows that organ-specific cancer rates correlate negatively with an organ's evolutionary antiquity. Although the relationship may just be coincidental, it suggests the possibility that recently-evolved differentiation states may be intricnsically more vulnerable to neoplastic change. Extrapolation of the regression line to a cancer incidence of zero equates to a level of tissue organization typical of 660 Myr ago; the inferred beginning of neoplasia therefore coincides with the rise of complex multicellular animals.