Hepcidin levels and gastric cancer risk in the EPIC-EurGast study.
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Authors
Jakszyn, PaulaFonseca-Nunes, Ana
Lujan-Barroso, Leila
Aranda, Núria
Tous, Mónica
Arija, Victoria
Cross, Amanda
Bueno-de-Mesquita, H B As
Weiderpass, Elisabete
Kühn, Tilman
Kaaks, Rudolf
Sjöberg, Klas
Ohlsson, Bodil
Tumino, Rosario
Palli, Domenico
Ricceri, Fulvio
Fasanelli, Francesca
Krogh, Vittorio
Mattiello, Amalia
Jenab, Mazda
Gunter, Marc
Perez-Cornago, Aurora
Khaw, Kay-Tee
Tjønneland, Anne
Olsen, Anja
Overvad, Kim
Trichopoulou, Antonia
Peppa, Eleni
Vasilopoulou, Effie
Boeing, Heiner
Sánchez-Cantalejo, Emilio
Huerta, José María
Dorronsoro, Miren
Barricarte, Aurelio
Quirós, José Maria
Peeters, Petra H
Agudo, Antonio
Type
ArticleLanguage
en
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Show full item recordTitle
Hepcidin levels and gastric cancer risk in the EPIC-EurGast study.Published in
Int J Cancer 2017; 141(5):945-51Publiekssamenvatting
Hepcidin is the main regulator of iron homeostasis and dysregulation of proteins involved in iron metabolism has been associated with tumorogenesis. However, to date, no epidemiological study has researched the association between hepcidin levels and gastric cancer risk. To further investigate the relationship between hepcidin levels and gastric cancer risk, we conducted a nested case-control study (EURGAST) within the multicentric European Prospective Investigation into Cancer and Nutrition study. The study included 456 primary incident gastric adenocarcinoma cases and 900 matched controls that occurred during an average of 11 years of follow-up. We measured serum levels of hepcidin-25, iron, ferritin, transferrin and C-reactive protein. Odds ratios (ORs) and 95% confidence intervals (CIs) for the risk of gastric cancer by hepcidin levels were estimated from multivariable conditional logistic regression models. Mediation effect of the ferritin levels on the hepcidin-gastric cancer pathway was also evaluated. After adjusting for relevant confounders, we observed a statistically significant inverse association between gastric cancer and hepcidin levels (OR 5 ng/l = 0.96, 95% CI = 0.93-0.99). No differences were found by tumor localization or histological type. In mediation analysis, we found that the direct effect of hepcidin only represents a nonsignificant 38% (95% CI: -69%, 91%). In summary, these data suggest that the inverse association of hepcidin levels and gastric cancer risk was mostly accounted by ferritin levels. Further investigation including repeated measures of hepcidin is needed to clarify their role in gastric carcinogenesis.PMID
28543377ae974a485f413a2113503eed53cd6c53
10.1002/ijc.30797
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