Liang Chen1, Zhigang Duan2, Lesley Tinker3, Haleh Sangi-Haghpeykar4, Howard Strickler5, Gloria Y F Ho5, Marc J Gunter6, Thomas Rohan5, Craig Logsdon7, Donna L White8, Kathryn Royse1, Hashem B El-Serag9, Li Jiao10. 1. Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael. E DeBakey VA Medical Center, Houston, TX, USA; Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX, USA. 2. Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael. E DeBakey VA Medical Center, Houston, TX, USA; Michael E. DeBakey VA Medical Center, Houston, TX, USA. 3. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. 4. Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX, USA. 5. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA. 6. Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom. 7. Department of Cancer Biology, Department of GI Medical Oncology, University of Texas, M. D. Anderson Cancer Center, Houston, TX, USA. 8. Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael. E DeBakey VA Medical Center, Houston, TX, USA; Texas Medical Center Digestive Disease Center, Houston, TX, USA; Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX, USA; Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX, USA; Michael E. DeBakey VA Medical Center, Houston, TX, USA. 9. Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael. E DeBakey VA Medical Center, Houston, TX, USA; Texas Medical Center Digestive Disease Center, Houston, TX, USA; Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX, USA; Michael E. DeBakey VA Medical Center, Houston, TX, USA. 10. Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael. E DeBakey VA Medical Center, Houston, TX, USA; Texas Medical Center Digestive Disease Center, Houston, TX, USA; Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, TX, USA; Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX, USA; Michael E. DeBakey VA Medical Center, Houston, TX, USA. Electronic address: jiao@bcm.edu.
Abstract
OBJECTIVES: Receptor for advanced glycation end products (RAGE) expressed on adipocytes and immune cells can bind to ligand N(ε)-(carboxymethyl)-lysine (CML) and trigger dysregulation of adipokines and chronic inflammation. Soluble RAGE (sRAGE) mitigates the detrimental effect of RAGE. We examined the associations between circulating levels of CML-AGE and sRAGE and colorectal cancer (CRC). METHODS: In a case-cohort study of the Women's Health Initiative Study, blood levels of CML-AGE and sRAGE were measured using ELISA. We used multivariable Cox regression model to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of incident CRC in relation to quartiles (Q) of biomarker levels. RESULTS: Average follow-up was 7.8 years for 444 cases and 805 subcohort members. In the subcohort, CML-AGE and sRAGE were inversely correlated with BMI (P values<0.0001). Levels of CML-AGE and sRAGE were not associated with CRC. In BMI-specific analysis, the association between sRAGE and CRC was observed. Among women with BMI≥25kg/m(2), those with highest levels of sRAGE had significantly lower risk for CRC as compared to women with lowest levels of sRAGE (HRQ4versusQ1: 0.39; 95% CI: 0.17-0.91). This inverse association was not observed among women with BMI <25kg/m(2) (P value for interaction=0.01). CONCLUSIONS: Among postmenopausal women, the RAGE pathway may be involved in obesity-related CRC.
OBJECTIVES:Receptor for advanced glycation end products (RAGE) expressed on adipocytes and immune cells can bind to ligand N(ε)-(carboxymethyl)-lysine (CML) and trigger dysregulation of adipokines and chronic inflammation. Soluble RAGE (sRAGE) mitigates the detrimental effect of RAGE. We examined the associations between circulating levels of CML-AGE and sRAGE and colorectal cancer (CRC). METHODS: In a case-cohort study of the Women's Health Initiative Study, blood levels of CML-AGE and sRAGE were measured using ELISA. We used multivariable Cox regression model to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of incident CRC in relation to quartiles (Q) of biomarker levels. RESULTS: Average follow-up was 7.8 years for 444 cases and 805 subcohort members. In the subcohort, CML-AGE and sRAGE were inversely correlated with BMI (P values<0.0001). Levels of CML-AGE and sRAGE were not associated with CRC. In BMI-specific analysis, the association between sRAGE and CRC was observed. Among women with BMI≥25kg/m(2), those with highest levels of sRAGE had significantly lower risk for CRC as compared to women with lowest levels of sRAGE (HRQ4versusQ1: 0.39; 95% CI: 0.17-0.91). This inverse association was not observed among women with BMI <25kg/m(2) (P value for interaction=0.01). CONCLUSIONS: Among postmenopausal women, the RAGE pathway may be involved in obesity-related CRC.
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