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@article{Dashti:2020:10.1158/1055-9965.EPI-20-0965,
author = {Dashti, SG and English, DR and Simpson, JA and Karahalios, A and Moreno-Betancur, M and Biessy, C and Rinaldi, S and Ferrari, P and Tjønneland, A and Halkjær, J and Dahm, CC and Vistisen, HT and Menegaux, F and Perduca, V and Severi, G and Aleksandrova, K and Schulze, MB and Masala, G and Sieri, S and Tumino, R and Macciotta, A and Panico, S and Hiensch, AE and May, AM and Quirós, JR and Agudo, A and Sánchez, M-J and Amiano, P and Colorado-Yohar, S and Ardanaz, E and Allen, NE and Weiderpass, E and Fortner, RT and Christakoudi, S and Tsilidis, KK and Riboli, E and Kaaks, R and Gunter, MJ and Viallon, V and Dossus, L},
doi = {10.1158/1055-9965.EPI-20-0965},
journal = {Cancer Epidemiology, Biomarkers and Prevention},
pages = {104--113},
title = {Adiposity and endometrial cancer risk in postmenopausal women: a sequential causal mediation analysis},
url = {http://dx.doi.org/10.1158/1055-9965.EPI-20-0965},
volume = {30},
year = {2020}
}

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TY  - JOUR
AB  - BACKGROUND: Adiposity increases endometrial cancer risk, possibly through inflammation, hyperinsulinemia, and increasing estrogens. We aimed to quantify the mediating effects of adiponectin (anti-inflammatory adipocytokine); IL6, IL1-receptor antagonist, TNF receptor 1 and 2, and C-reactive protein (inflammatory status biomarkers); C-peptide (hyperinsulinemia biomarker); and free estradiol and estrone (estrogen biomarkers) in the adiposity-endometrial cancer link in postmenopausal women. METHODS: We used data from a case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC). Eligible women did not have cancer, hysterectomy, and diabetes; did not use oral contraceptives or hormone therapy; and were postmenopausal at recruitment. Mediating pathways from adiposity to endometrial cancer were investigated by estimating natural indirect (NIE) and direct (NDE) effects using sequential mediation analysis. RESULTS: The study included 163 cases and 306 controls. The adjusted OR for endometrial cancer for body mass index (BMI) ≥30 versus ≥18.5-<25 kg/m2 was 2.51 (95% confidence interval, 1.26-5.02). The ORsNIE were 1.95 (1.01-3.74) through all biomarkers [72% proportion mediated (PM)] decomposed as: 1.35 (1.06-1.73) through pathways originating with adiponectin (33% PM); 1.13 (0.71-1.80) through inflammation beyond (the potential influence of) adiponectin (13% PM); 1.05 (0.88-1.24) through C-peptide beyond adiponectin and inflammation (5% PM); and 1.22 (0.89-1.67) through estrogens beyond preceding biomarkers (21% PM). The ORNDE not through biomarkers was 1.29 (0.54-3.09). Waist circumference gave similar results. CONCLUSIONS: Reduced adiponectin and increased inflammatory biomarkers, C-peptide, and estrogens mediated approximately 70% of increased odds of endometrial cancer in women with obesity versus normal weight. IMPACT: If replicated, these results could have implications for identifying targets for intervention to reduce e
AU  - Dashti,SG
AU  - English,DR
AU  - Simpson,JA
AU  - Karahalios,A
AU  - Moreno-Betancur,M
AU  - Biessy,C
AU  - Rinaldi,S
AU  - Ferrari,P
AU  - Tjønneland,A
AU  - Halkjær,J
AU  - Dahm,CC
AU  - Vistisen,HT
AU  - Menegaux,F
AU  - Perduca,V
AU  - Severi,G
AU  - Aleksandrova,K
AU  - Schulze,MB
AU  - Masala,G
AU  - Sieri,S
AU  - Tumino,R
AU  - Macciotta,A
AU  - Panico,S
AU  - Hiensch,AE
AU  - May,AM
AU  - Quirós,JR
AU  - Agudo,A
AU  - Sánchez,M-J
AU  - Amiano,P
AU  - Colorado-Yohar,S
AU  - Ardanaz,E
AU  - Allen,NE
AU  - Weiderpass,E
AU  - Fortner,RT
AU  - Christakoudi,S
AU  - Tsilidis,KK
AU  - Riboli,E
AU  - Kaaks,R
AU  - Gunter,MJ
AU  - Viallon,V
AU  - Dossus,L
DO  - 10.1158/1055-9965.EPI-20-0965
EP  - 113
PY  - 2020///
SN  - 1055-9965
SP  - 104
TI  - Adiposity and endometrial cancer risk in postmenopausal women: a sequential causal mediation analysis
T2  - Cancer Epidemiology, Biomarkers and Prevention
UR  - http://dx.doi.org/10.1158/1055-9965.EPI-20-0965
UR  - https://www.ncbi.nlm.nih.gov/pubmed/33008875
UR  - https://cebp.aacrjournals.org/content/30/1/104
UR  - http://hdl.handle.net/10044/1/84241
VL  - 30
ER  -

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