Chen Yuan1, Vicente Morales-Oyarvide1, Natalia Khalaf2, Kimberly Perez1, Fred K Tabung3,4,5, Gloria Y F Ho6, Charles Kooperberg7, Aladdin H Shadyab8, Lihong Qi9, Peter Kraft10,11, Howard D Sesso10,12,13, Edward L Giovannucci5,10,13, JoAnn E Manson10,12, Meir J Stampfer5,10,13, Kimmie Ng1, Charles S Fuchs14, Brian M Wolpin1, Ana Babic1. 1. Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA. 2. Department of Medicine, Section of Gastroenterology and Hepatology, Baylor College of Medicine, Houston, TX, USA. 3. Division of Medical Oncology, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, OH, USA. 4. The Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Columbus, OH, USA. 5. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 6. Department of Occupational Medicine, Epidemiology and Prevention, Feinstein Institute for Medical Research, Northwell Health, Great Neck, NY, USA. 7. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. 8. Division of Epidemiology, Department of Family Medicine and Public Health, University of California San Diego School of Medicine, La Jolla, CA, USA. 9. Division of Biostatistics, Department of Public Health Sciences, University of California Davis School of Medicine, Davis, CA, USA. 10. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 11. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA. 12. Division of Preventive Medicine and Division of Aging, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 13. Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. 14. Yale Cancer Center, Smilow Cancer Hospital, New Haven, CT, USA.
Abstract
BACKGROUND: Chronic inflammation may promote initiation and progression of pancreatic cancer, but no studies have examined the association between inflammation in the period before diagnosis and pancreatic cancer survival. METHODS: We prospectively examined the association of prediagnostic plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 2 with survival among 492 participants from 5 large US prospective cohort studies who developed pancreatic cancer. Using an empirical dietary inflammatory pattern (EDIP) score, we evaluated whether long-term proinflammatory diets were associated with survival among 1153 patients from 2 of the 5 cohorts. Cox proportional hazards regression was used to estimate hazard ratios for death with adjustment for potential confounders. All statistical tests were 2-sided. RESULTS: Higher prediagnostic levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 2 were individually associated with reduced survival (Ptrend = .03, .01, and .04, respectively). Compared with patients with a combined inflammatory biomarker score of 0 (all 3 marker levels below medians), those with a score of 3 (all 3 marker levels above medians) had a hazard ratio for death of 1.57 (95% confidence interval = 1.16 to 2.12; Ptrend = .003), corresponding to median overall survival times of 8 vs 5 months. Patients consuming the most proinflammatory diets (EDIP quartile 4) in the prediagnostic period had a hazard ratio for death of 1.34 (95% confidence interval = 1.13 to 1.59; Ptrend = .01), compared with those consuming the least proinflammatory diets (EDIP quartile 1). CONCLUSION: Prediagnostic levels of inflammatory biomarkers and long-term proinflammatory diets were inversely associated with pancreatic cancer survival.
BACKGROUND: Chronic inflammation may promote initiation and progression of pancreatic cancer, but no studies have examined the association between inflammation in the period before diagnosis and pancreatic cancer survival. METHODS: We prospectively examined the association of prediagnostic plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 2 with survival among 492 participants from 5 large US prospective cohort studies who developed pancreatic cancer. Using an empirical dietary inflammatory pattern (EDIP) score, we evaluated whether long-term proinflammatory diets were associated with survival among 1153 patients from 2 of the 5 cohorts. Cox proportional hazards regression was used to estimate hazard ratios for death with adjustment for potential confounders. All statistical tests were 2-sided. RESULTS: Higher prediagnostic levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 2 were individually associated with reduced survival (Ptrend = .03, .01, and .04, respectively). Compared with patients with a combined inflammatory biomarker score of 0 (all 3 marker levels below medians), those with a score of 3 (all 3 marker levels above medians) had a hazard ratio for death of 1.57 (95% confidence interval = 1.16 to 2.12; Ptrend = .003), corresponding to median overall survival times of 8 vs 5 months. Patients consuming the most proinflammatory diets (EDIP quartile 4) in the prediagnostic period had a hazard ratio for death of 1.34 (95% confidence interval = 1.13 to 1.59; Ptrend = .01), compared with those consuming the least proinflammatory diets (EDIP quartile 1). CONCLUSION: Prediagnostic levels of inflammatory biomarkers and long-term proinflammatory diets were inversely associated with pancreatic cancer survival.
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