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Hemochromatosis gene mutations among Finnish male breast and prostate cancer patients
Author(s) -
Syrjäkoski Kirsi,
Fredriksson Henna,
Ikonen Tarja,
Kuukasjärvi Tuula,
Autio Ville,
Matikainen Mika P.,
Tammela Teuvo L.J.,
Koivisto Pasi A.,
Schleutker Johanna
Publication year - 2006
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.21331
Subject(s) - hemochromatosis , medicine , hereditary hemochromatosis , breast cancer , population , cancer , male breast cancer , prostate cancer , genetic predisposition , oncology , gastroenterology , genetics , disease , biology , environmental health
Hereditary hemochromatosis (HH), the most common genetic disease in northern Europeans, is an autosomal recessive disorder of iron metabolism. The association between hepatocellular carcinoma and HFE homozygosity is well documented, but recently HFE hetero‐ and homozygosity has also been linked to nonhepatocellular malignancies, including female breast cancer. We hypothesized that C282Y and H63D mutations in the HFE gene could contribute to male breast cancer (MBC) and prostate cancer (PC) susceptibility at the population level in Finland. We screened the 2 major HFE mutations, H63D and C282Y, from 116 MBC cases diagnosed in Finland between 1967 and 1996, 843 consecutive unselected PC cases diagnosed at the Pirkanmaa Hospital District between 1999 and 2001 and 480 anonymous blood donor controls by minisequencing. Our results indicate that the frequencies of the HFE mutations do not significantly differ between MBC and PC patients and the population‐based controls. No significantly altered risks for MBC or PC among carriers of the 2 variants were observed. However, HFE mutations were seen twice as often among carriers of a common BRCA2 mutation 9346(−2)A→G compared with the rest of the MBC cases, indicating that HFE may be an MBC risk modifier gene among BRCA2 mutation carriers. In conclusion, our results indicate a minor role for the HFE mutations C282Y and H63D in the causation of MBC and PC, but carriers of both BRCA2 9346(−2)A→G and an HFE mutation may be at an increased risk. © 2005 Wiley‐Liss, Inc.