Age has long been known as the primary population 'risk factor' for cancer. We suggest that the observed disparities in hormonal cancers by ethnicity, gender, and other indices of social structure and power relationships, imply a differential aging by psychosocial and environmental exposures, in the context of cross-generational epigenetic heritage. A relatively simple model of malignancy regulation illuminates the cellular root of induced aging, and explains the decline in cancer rate with extreme old age via telomere shortening. We find that the multifactorial determinants of the disorder cannot be effectively addressed by 'small molecule' interventions at the individual level, but must involve comprehensive prevention strategies that lessen exposures to policies and cultural practices that accelerate senescence in vulnerable or targeted populations
