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Search Results for all work with filters:

  • Agnoli, Claudia
  • Trichopoulou, Antonia
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Work 1-3 of 3

Sorted by relevance

Article

Inflammatory and Metabolic Biomarkers and Risk of Liver and Biliary Tract Cancer

by Krasimira Aleksandrova; Heiner Boeing; Ute Nöthlings; Mazda Jenab; Veronika Fedirko; Rudolf Kaaks; Annekatrin Lukanova; Antonia Trichopoulou; Dimitrios Trichopoulos; Paolo Boffetta; Elisabeth Trepo; Sabine Westhpal; Talita Duarte-Salles; Magdalena Stepien; Kim Overvad; Anne Tjønneland; Jytte Halkjær; Marie-Christine Boutron-Ruault; Laure Dossus; Antoine Racine; Pagona Lagiou; Christina Bamia; Vassiliki Benetou; Claudia Agnoli; Domenico Palli; Salvatore Panico; Rosario Tumino; Paolo Vineis; Bas Bueno-De-Mesquita; Petra H Peeters; Inger Torhild Gram; Eiliv Lund; Elisabete Weiderpass; J Ramón Quirós; Antonio Agudo; María-José Sánchez; Diana Gavrila; Aurelio Barricarte; Miren Dorronsoro; Bodil Ohlsson; Björn Lindkvist; Anders Johansson; Malin Sund; Kay-Tee Khaw; Nicholas Wareham; Ruth C Travis; Elio Riboli; Tobias Pischon

2014

Subjects
  • Health Sciences, Epidemiology
  • Health Sciences, Public Health
  • File Download
  • View Abstract

Abstract:Close

Obesity and associated metabolic disorders have been implicated in liver carcinogenesis; however, there are little data on the role of obesity-related biomarkers on liver cancer risk. We studied prospectively the association of inflammatory and metabolic biomarkers with risks of hepatocellular carcinoma (HCC), intrahepatic bile duct (IBD), and gallbladder and biliary tract cancers outside of the liver (GBTC) in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition. Over an average of 7.7 years, 296 participants developed HCC (n=125), GBTC (n=137), or IBD (n=34). Using risk-set sampling, controls were selected in a 2:1 ratio and matched for recruitment center, age, sex, fasting status, and time of blood collection. Baseline serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), C-peptide, total high-molecular-weight (HMW) adiponectin, leptin, fetuin-a, and glutamatdehydrogenase (GLDH) were measured, and incidence rate ratios (IRRs) and 95% confidence intervals (CIs) were estimated using conditional logistic regression. After adjustment for lifestyle factors, diabetes, hepatitis infection, and adiposity measures, higher concentrations of CRP, IL-6, C-peptide, and non-HMW adiponectin were associated with higher risk of HCC (IRR per doubling of concentrations=1.22; 95% CI=1.02-1.46; P = 0.03; 1.90; 95% CI=1.30-2.77; P = 0.001; 2.25; 95% CI=1.43-3.54; P = 0.0005; and 2.09; 95% CI=1.19-3.67; P = 0.01, respectively). CRP was associated also with risk of GBTC (IRR=1.22; 95% CI=1.05-1.42; P = 0.01). GLDH was associated with risks of HCC (IRR=1.62; 95% CI=1.25-2.11; P = 0.0003) and IBD (IRR=10.5; 95% CI=2.20-50.90; P = 0.003). The continuous net reclassification index was 0.63 for CRP, IL-6, C-peptide, and non-HMW adiponectin and 0.46 for GLDH, indicating good predictive ability of these biomarkers. Conclusion: Elevated levels of biomarkers of inflammation and hyperinsulinemia are associated with a higher risk of HCC, independent of obesity and established liver cancer risk factors.

Conference

Association of Selenoprotein and Selenium Pathway Genotypes with Risk of Colorectal Cancer and Interaction with Selenium Status

by Veronika Fedirko; Mazda Jenab; Catherine Meplan; Jeb Jones; Wanzhe Zhu; Lutz Schomburg; Afshan Siddiq; Sandra Hybsier; Kim Overvad; Anne Tjonneland; Hanane Omichessan; Vittorio Perduca; Marie-Christine Boutron-Ruault; Tilman Kuehn; Verena Katzke; Krasimira Aleksandrova; Antonia Trichopoulou; Anna Karakatsani; Anastasia Kotanidou; Rosario Tumino; Salvatore Panico; Giovanna Masala; Claudia Agnoli; Alessio Naccarati; Bas Bueno-de-Mesquita; Roel C.H. Vermeulen; Elisabete Weiderpass; Guri Skeie; Therese Haugdahl Nost; Leila Lujan-Barroso; J. Ramon Quiros; Jose Maria Huerta; Miguel Rodriguez-Barranco; Aurelio Barricarte; Bjorn Gylling; Sophia Harlid; Kathryn E. Bradbury; Nick Wareham; Kay-Tee Khaw; Marc Gunter; Neil Murphy; Heinz Freisling; Kostas Tsilidis; Dagfinn Aune; Elio Riboli; John E. Hesketh; David J. Hughes

2019-04-01

Subjects
  • Health Sciences, Epidemiology
  • Health Sciences, Oncology
  • Health Sciences, Nutrition
  • File Download
  • View Abstract

Abstract:Close

Selenoprotein genetic variations and suboptimal selenium (Se) levels may contribute to the risk of colorectal cancer (CRC) development. We examined the association between CRC risk and genotype for single nucleotide polymorphisms (SNPs) in selenoprotein and Se metabolic pathway genes. Illumina Goldengate assays were designed and resulted in the genotyping of 1040 variants in 154 genes from 1420 cases and 1421 controls within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Multivariable logistic regression revealed an association of 144 individual SNPs from 63 Se pathway genes with CRC risk. However, regarding the selenoprotein genes, only TXNRD1 rs11111979 retained borderline statistical significance after adjustment for correlated tests (PACT = 0.10; PACT significance threshold was P < 0.1). SNPs in Wingless/Integrated (Wnt) and Transforming growth factor (TGF) beta-signaling genes (FRZB, SMAD3, SMAD7) from pathways affected by Se intake were also associated with CRC risk after multiple testing adjustments. Interactions with Se status (using existing serum Se and Selenoprotein P data) were tested at the SNP, gene, and pathway levels. Pathway analyses using the modified Adaptive Rank Truncated Product method suggested that genes and gene x Se status interactions in antioxidant, apoptosis, and TGF-beta signaling pathways may be associated with CRC risk. This study suggests that SNPs in the Se pathway alone or in combination with suboptimal Se status may contribute to CRC development.

Article

Circulating concentrations of vitamin D in relation to pancreatic cancer risk in European populations

by Franzel J.B. van Duijnhoven; Mazda Jenab; Kristian Hveem; Peter D. Siersema; Veronika Fedirko; Eric J. Duell; Ellen Kampman; Anouk Halfweeg; Henk J. van Kranen; Jody M.W. van den Ouweland; Elisabete Weiderpass; Neil Murphy; Arnulf Langhammer; Eivind Ness-Jensen; Anja Olsen; Anne Tjonneland; Kim Overvad; Claire Cadeau; Marina Kvaskoff; Marie-Christine Boutron-Ruault; Verena A. Katzke; Tilman Kuehn; Heiner Boeing; Antonia Trichopoulou; Anastasia Kotanidou; Maria Kritikou; Domenico Palli; Claudia Agnoli; Rosario Tumino; Salvatore Panico; Giuseppe Matullo; Petra Peeters; Magritt Brustad; Karina Standahl Olsen; Cristina Lasheras; Mireia Obon-Santacana; Maria-Jose Sanchez; Miren Dorronsoro; Maria-Dolores Chirlaque; Aurelio Barricarte; Jonas Manjer; Martin Almquist; Frida Renstrom; Weimin Ye; Nick Wareham; Kay-Tee Khaw; Kathryn E. Bradbury; Heinz Freisling; Dagfinn Aune; Teresa Norat; Elio Riboli; H. B(as) Bueno-de-Mesquita

2018

Subjects
  • Health Sciences, Epidemiology
  • Health Sciences, Public Health
  • File Download
  • View Abstract

Abstract:Close

Evidence from in vivo, in vitro and ecological studies are suggestive of a protective effect of vitamin D against pancreatic cancer (PC). However, this has not been confirmed by analytical epidemiological studies. We aimed to examine the association between pre-diagnostic circulating vitamin D concentrations and PC incidence in European populations. We conducted a pooled nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) and the Nord-Trøndelag Health Study's second survey (HUNT2) cohorts. In total, 738 primary incident PC cases (EPIC n = 626; HUNT2 n = 112; median follow-up = 6.9 years) were matched to 738 controls. Vitamin D [25(OH)D 2 and 25(OH)D 3 combined] concentrations were determined using isotope-dilution liquid chromatography-tandem mass spectrometry. Conditional logistic regression models with adjustments for body mass index and smoking habits were used to estimate incidence rate ratios (IRRs) and 95% confidence intervals (95%CI). Compared with a reference category of > 50 to 75 nmol/L vitamin D, the IRRs (95% CIs) were 0.71 (0.42–1.20); 0.94 (0.72–1.22); 1.12 (0.82–1.53) and 1.26 (0.79–2.01) for clinically pre-defined categories of ≤25; > 25 to 50; > 75 to 100; and > 100 nmol/L vitamin D, respectively (p for trend = 0.09). Corresponding analyses by quintiles of season-standardized vitamin D concentrations also did not reveal associations with PC risk (p for trend = 0.23). Although these findings among participants from the largest combination of European cohort studies to date show increasing effect estimates of PC risk with increasing pre-diagnostic concentrations of vitamin D, they are not statistically significant.
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