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HFE H63D variant and leukemia

Lookup NU author(s): Dr Tevfik Dorak


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(First Paragraph) The hereditary hemochromatosis gene HFE is one of many genes involved in iron homeostasis. Because of the known effects of iron on carcinogenesis, any genetic variation including those in HFE that increases body iron content may raise cancer risk. A strong epidemiologic connection between serum iron levels and long-term general cancer risk has been demonstrated mainly by Richard Stevens [1]. The first genetic risk assessment by Beckman's group in Sweden revealed an interaction between HFE C282Y mutation and transferrin receptor gene (TFRC) variant S142G in multiple myeloma, breast and colorectal cancers, and hepatocellular carcinoma [2]. Further studies have continued to show associations with single gene variants or gene and environment (C282Y or H63D x diet) interactions. Breast cancer, for example, has been associated with increased risk conferred by gene and gene interaction (C282Y x S142G) in Sweden [2], C282Y in USA [3], and H63D in Russia [4] and Turkey [5]. In colorectal cancer, associations with single gene variants (C282Y or H63D) [6] or compound heterozygosity (C282Y/H63D) [7], gene and gene (C282Y x S142G) [8] or gene and environment (C282Y x iron-rich diet) interactions [6] have been reported as risk markers. Even though a number of negative results have also been published, a picture may be emerging of different variants having variable penetrance in different populations in terms of their effect on body iron status and their associations varying in strength.

Publication metadata

Author(s): Dorak MT

Publication type: Article

Publication status: Published

Journal: Leukemia & Lymphoma

Year: 2006

Volume: 47

Issue: 11

Pages: 2269-2270

Print publication date: 01/01/2006

ISSN (print): 1042-8194

ISSN (electronic): 1026-8022

Publisher: Informa Healthcare


DOI: 10.1080/10428190600834461


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