Four epidemiological studies have been performed that are generally consistent with the hypothesis that increased available body iron stores increase the risk of cancer or of general mortality. In a study based on the First National Health and Nutrition Examination Survey in the United States (NHANES), 232 men who developed cancer over a ten year period had a mean transferrin saturation of 33.1% at least 4 years before diagnosis, whereas 3,113 men who did not develop cancer had a transferrin saturation of 30.7% (p = 0.002). The hypothesis is based on two possible biological mechanisms. First, iron can catalyse the production of oxygen radicals and these may be proximate carcinogens. Second, iron may be a limiting nutrient to the growth and replication of a cancer cell. There are at least five areas of potential research related to iron and cancer based on these biological mechanisms: (1) etiology of cancer, (2) etiology of radiation-induced cancer, (3) prognosis after cancer diagnosis, (4) cancer risk resulting from therapy, and (5) interactions with other biochemical factors. An unexpected finding of the human studies done to date has been a highly significant negative association of serum albumin and long term cancer risk. Serum albumin is lower in smokers and older people, however, the negative association persists after controlling for these factors.