Iron in neoplastic disease.
Normal and neoplastic cells have similar needs for iron, but the latter may exhibit altered mechanisms of iron acquisition that permit continued multiplication in host iron-restricted tissues. For example, neoplastic cells may form low molecular weight siderophores as well as increase the number of transferrin binding glycoproteins on their cell surfaces. The hosts attempt to withhold iron from neoplastic cells by preventing the return of the metal to plasma and diverting it to storage, by increasing the synthesis of ferritin to accommodate the added stores, and by surrounding tumor cells with macrophages that can ingest lactoferrin-bound iron, but these mechanisms are often not effective against the iron-accumulating mechanisms of the tumor. Persons or animals with iron overload (via ingestion, inhalation, injection, or pathophysiologic process) tend to be at greater risk than normal hosts in the development of neoplasms. The tumors are often associated with the site(s) of deposition of the metal. In addition to its neoplastic cell nutrient function, excess iron might suppress tumorcidal action of macrophages and interfere with lymphocyte traffic. Severe iron deficiency can interfere with the ability of the host to detoxify potential carcinogens as well as with its ability to activate antitumor lymphocytes.
D000818:Animals; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced; D005260:Female; D006801:Humans; D007501:Iron / Q000009:adverse effects / Q000378:metabolism*; D008113:Liver Neoplasms / Q000139:chemically induced; D008297:Male; D051379:Mice; D009369:Neoplasms / Q000139:chemically induced / Q000378:metabolism*; D009751:Nutritional Requirements; D011471:Prostatic Neoplasms / Q000378:metabolism; D051381:Rats; D014168:Transferrin / Q000378:metabolism
D014168:Transferrin; D007501:Iron