Iron excess and cancer

Abstract

In the last two decades, strong observational and experimental evidence has been presented for the role of iron excess in cancer development. The hereditary hemochromatosis gene HFE variants that increase body iron levels are associated with increased cancer risk. The first such association was reported by us in childhood acute lymphoblastic leukemia. With the identification of molecular mechanisms of potentiation of carcinogenesis by iron, epidemiologic associations have been gaining more weight. Experimental data also increase the credibility of suggestions that iron excess can both initiate (genotoxic effect) and promote (via its effect on immune function) cancer development. Both environmental and genetic factors may lead to iron excess but the effect is strongest in combination. Iron excess may contribute to cancer development in many different ways, most of which yet unappreciated and most relevant of those possible connections are discussed in this chapter. Since reduction in smoking, alcohol and red meat consumption eliminates excessive exposure to iron, eating fruits and vegetables does not expose the body to too much bioavailable iron and perhaps replaces other iron-rich food stuff and avoidance of excess iron levels reduces infections, iron is indirectly involved in the success of these preventive measures. Perhaps it is time to emphasize lower exposure to environmental iron directly as an important factor to reduce the cancer burden in the industrialized world. © 2010 Springer Science+Business Media, LLC.