RT Journal Article
T1 Hepcidin levels and gastric cancer risk in the EPIC-EurGast study.
A1 Jakszyn, Paula
A1 Fonseca-Nunes, Ana
A1 Lujan-Barroso, Leila
A1 Aranda, Núria
A1 Tous, Mónica
A1 Arija, Victoria
A1 Cross, Amanda
A1 Bueno-de-Mesquita, H B As
A1 Weiderpass, Elisabete
A1 Kühn, Tilman
A1 Kaaks, Rudolf
A1 Sjöberg, Klas
A1 Ohlsson, Bodil
A1 Tumino, Rosario
A1 Palli, Domenico
A1 Ricceri, Fulvio
A1 Fasanelli, Francesca
A1 Krogh, Vittorio
A1 Mattiello, Amalia
A1 Jenab, Mazda
A1 Gunter, Marc
A1 Perez-Cornago, Aurora
A1 Khaw, Kay-Tee
A1 Tjønneland, Anne
A1 Olsen, Anja
A1 Overvad, Kim
A1 Trichopoulou, Antonia
A1 Peppa, Eleni
A1 Vasilopoulou, Effie
A1 Boeing, Heiner
A1 Sánchez-Cantalejo, Emilio
A1 Huerta, José María
A1 Dorronsoro, Miren
A1 Barricarte, Aurelio
A1 Quirós, José Maria
A1 Peeters, Petra H
A1 Agudo, Antonio
K1 cohort study
K1 gastric cancer
K1 hepcidin
K1 iron homeostasis
AB 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.
YR 2017
FD 2017-06-21
LK http://hdl.handle.net/10668/11238
UL http://hdl.handle.net/10668/11238
LA en
DS RISalud
RD Apr 18, 2025