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Utilizing its genetics platform, Xenon's discovery of the genes underlying the rare genetic disorder juvenile hemochromatosis (JH) led to its selection of hepcidin, a protein produced in the liver, as a drug target to treat patients with ACD.
Juvenile hemochromatosis (JH) is due to a mutation in 1 of 2 genes: HFE2 [hemochromatosis type 2 (juvenile); also known as HJV and encoding hemojuvelin] (7) and, more rarely, HAMP (hepcidin antimicrobial peptide) (8).
With Xenon he has also identified genes associated with rare disorders such as Tangier disease, juvenile hemochromatosis and congenital insensitivity to pain.
Juvenile hemochromatosis locus maps to chromosome 1q.
The recent identification of two mutations (Y250X and E60X) in the TFR2 gene of Italian hemochromatosis probands lacking HFE mutations (30) and the mapping of the juvenile hemochromatosis gene on 1821 (31) argue for the heterogeneity of the disease and indicate that mutations in genes other than HFE can be associated with hemochromatosis.
Although hereditary, juvenile hemochromatosis is considered a separate disease from hereditary hemochromatosis.