Most experimental and human data support the hypothesis that iron overload
is a risk factor for cancer in general and liver cancer in particular. This
oncogenic effect could be explained by an overproduction of reactive oxyge
n species and free radicals. in cirrhosis due to genetic haemochromatosis (
homozygosity for the mutation C282 Y in the HFE gene) there is an increase
incidence of hepatocellular carcinoma. Few cases have been reported in gene
tic haemochromatosis with iron overload but without cirrhosis. In hepatocel
lular carcinoma developed in non cirrhotic liver there is a mild iron overl
oad iir more than 50 % of cases. In these patients heterozygous and compoun
d C282 Y mutations are found in 36 %. In black Africans, iron overload gene
tically determined but not linked to mutations in the HFE gene increases al
so the risk of hepatocellullar carcinoma. Among the many factors (viral hep
atitis, alcohol, tobacoo etc.) which play a role bl hepatic carcinogenesis
iron overload is probably an important one and therefore should be treated.