Investigation of Genetic Variants of Genes of the Hemochromatosis Pathway and Their Role in Breast Cancer

Abraham, Benny K.; Justenhoven, Christina; Pesch, Beate; Harth, Volker; Weirich, Gregor; Baisch, Christian; Rabstein, Sylvia; Ko, Yon‐Dschun; Brüning, Thomas; Fischer, Hans‐Peter; Haas, Susanne; Brod, Sandra; Oberkanins, Christian; Hamann, Ute; Brauch, Hiltrud

doi:10.1158/1055-9965.epi-05-0013

Cited by 33 publications

(33 citation statements)

References 27 publications

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“…Primarily, GENICA aimed to investigate gene-environment interactions (29)(30)(31) and contributes to the International Breast Cancer Association Consortium (32,33). When the first epidemiological results for night work as a potential risk factor for breast cancer were emerging, we added questions on shift work to our study.…”

Section: Discussionmentioning

confidence: 99%

Night work and breast cancer – results from the German GENICA study

Pesch¹,

Harth²,

Rabstein³

et al. 2009

Scand J Work Environ Health

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118

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Section: Discussionmentioning

confidence: 99%

Night work and breast cancer – results from the German GENICA study

Pesch¹,

Harth²,

Rabstein³

et al. 2009

Scand J Work Environ Health

Self Cite

118

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“…Heterozygous HFE carriership is associated with moderately increased iron parameters, and therefore, it has been suggested to be a genetic modifier of several clonal disorders (solid tumors and hematologic malignancies). Previous association studies regarding common HFE genetic variants in relation with susceptibility for solid tumors such as colon cancer (7,8,(14)(15)(16)(17), or breast cancer (9)(10)(11)18), are rather conflicting. HFE associations were investigated in hematologic malignancies as well.…”

Section: Discussionmentioning

confidence: 99%

“…The S142G variant of TFR was reported to influence cancer susceptibility (colon, breast, myeloma) in combination with distinct HFE genotypes (13). The effects of iron homeostasis, and HFE and TFR genotypes were extensively studied in several solid tumors even in large patient cohorts (7)(8)(9)(10)(11)(12)(14)(15)(16)(17)(18)), but only a few studies with small patient cohorts tested the potential role of HFE in chronic myeloproliferative disorders (CMPD), a clonal disorder of the main iron using tissue of the body (19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

HFEC282Y Mutation as a Genetic Modifier Influencing Disease Susceptibility for Chronic Myeloproliferative Disease

Andrikovics

Meggyesi

Szilvási

et al. 2009

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Iron metabolism has been implicated in carcinogenesis and several studies assessed the potential role of genetic variants of proteins involved in iron metabolism (HFE C282Y, TFR S142G) in different malignancies. Few reports addressed this issue with relation to chronic myeloproliferative disorders (CMPD). The aims of our study were (a) to examine the potential associations of CMPD development with genetic modifiers of iron metabolism in a large cohort of CMPD patients; (b) to examine associations of genetic variants of proteins involved in iron metabolism; and acquired JAK2 V617F mutation with clinical characteristics of CMPD. HFE C282Y was genotyped in 328 CMPD patients and 996 blood donors as controls, HFE H63D, and TFR S142G were tested in CMPD patients and 171 first time blood donors. JAK2 V617F mutation was tested in CMPD patients and in 122 repeated blood donors. Decreased C282Y allele frequency (allele frequency F 95% confidence interval) was found in the CMPD group (1.8% F 1.0%) compared with controls (3.4% F 0.8%; P = 0.048). TFR S142G allele frequency was reduced among V617F-negative CMPD patients (34.8% F7.6%) compared with controls (47.8% F 5.4%; P = 0.02). The frequency of JAK2 V617F was 75.9% (249 of 328) in the CMPD group. At presentation, elevated hemoglobin levels were found in V617F-positive patients compared with V617F-negative counterparts (P < 0.000). Vascular complications (26.6% versus 15.2%; P = 0.039) as well as female gender (57.4% versus 41.8%; P = 0.019) were more common in V617F-positive patients. We found that HFE C282Y might be associated with a protective role against CMPD. Because chronic iron deficiency or latent anemia may trigger disease susceptibility for CMPD, HFE C282Y positivity may be a genetic factor influencing this effect. (Cancer Epidemiol Biomarkers Prev 2009;18(3):929 -34)

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“…Kallianpur and others (68) concluded that HFE Tyr282 allele was more frequent in a group of cases with breast cancer from Tennessee in comparison with women from the same state or the general population (P < 0.001). These observations may be explained by the elevated cellular iron uptake associated with the HFE Tyr282 allele (69) or the high iron content in breast cancer cells (61). However, these observations are limited to a low number of patients (61,68).…”

Section: Breast Cancermentioning

confidence: 99%

“…These observations may be explained by the elevated cellular iron uptake associated with the HFE Tyr282 allele (69) or the high iron content in breast cancer cells (61). However, these observations are limited to a low number of patients (61,68).…”

Section: Breast Cancermentioning

confidence: 99%

The Dual Nature of Iron in Relation to Cancer: A Review

et al. 2016

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Background: Although iron is essential for all cells, it could be potentially hazardous. This is mostly due to iron participation in oxidation-reduction reactions. In terms of cancer risk, the role of both iron deficiency and overload can be studied in two directions, protective or therapeutic effects, and carcinogenic effects. Materials and Methods:PubMed, Science direct, Ovid, Proquest, Medline, and Google scholar databases were used to obtain articles identified by using the key words "Iron", "Iron deficiency", "Iron overload", "Cancer", and "Neoplasm" without any time limit. The relevance of studies was identified by reviewing the titles and the abstracts. 185 articles published in English, including experimental, observational, molecular and cellular studies were reviewed. Results and Conclusion:Considering the dual nature of iron, maintaining an optimal iron level in the body is important. This can be achieved when regulatory mechanisms of body iron level work properly and the amount of iron input is within the physiological range. Current evidence generally supports this possibility that higher animal-derived (heme) iron may increase the risk of some cancers. The release of iron or nitrosyl heme from iron complexes during some processing of meat may increase production of cancer promoter lipoperoxides. On the other hand, use of iron chelation or iron mediated oxidative assault for the treatment or prevention of cancer appears to be promising; but further research is required. Considering this background, this article reviews the literature and evidence, focusing on the role of iron overload and deficiency in developing and treatment of various cancers.

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Investigation of Genetic Variants of Genes of the Hemochromatosis Pathway and Their Role in Breast Cancer

Cited by 33 publications

References 27 publications

Night work and breast cancer – results from the German GENICA study

Night work and breast cancer – results from the German GENICA study

HFEC282Y Mutation as a Genetic Modifier Influencing Disease Susceptibility for Chronic Myeloproliferative Disease

The Dual Nature of Iron in Relation to Cancer: A Review

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