Joshua Demb1, Esther K Wei2, Monika Izano3, Stephen Kritchevsky4, Helen Swede5, Anne B Newman6, Michael Shlipak7, Tomi Akinyemiju8, Steven Gregorich9, Dejana Braithwaite10. 1. Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, United States; Department of Oncology, Georgetown University, Washington, DC, United States. Electronic address: Josh.demb@ucsf.edu. 2. California Pacific Medical Center Research Institute, San Francisco, CA, United States. Electronic address: WeiE@cpmcri.org. 3. Department of Epidemiology, University of California, Berkeley, CA, United States. 4. Wake Forest School of Medicine, Winston-Salem, NC, United States. Electronic address: skritche@wakehealth.edu. 5. Department of Community Medicine and Healthcare, University of Connecticut School of Medicine, Farmington, CT, United States. Electronic address: hswede@uchc.edu. 6. School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States. Electronic address: newmana@edc.pitt.edu. 7. Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, United States. Electronic address: Michael.Shlipak@ucsf.edu. 8. Department of Epidemiology, University of Kentucky, Lexington, KY, United States. Electronic address: tomiakin@uky.edu. 9. Department of Medicine, University of California, San Francisco, CA, United States. Electronic address: Steven.Gregorich@ucsf.edu. 10. Department of Oncology, Georgetown University, Washington, DC, United States. Electronic address: Dejana.Braithwaite@georgetown.edu.
Abstract
OBJECTIVES: We examined the association between three inflammatory markers (Interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α) and incident lung cancer using baseline, updated, and averaged inflammatory measures in older adults. METHODS: We fitted multivariable Cox models to assess whether circulating levels of inflammation markers were associated with incident lung cancers in the Health Aging, Body and Composition (HealthABC) prospective cohort of 3075 older adults aged 70-79 years at baseline. IL-6 and CRP were measured biennially, whereas TNF-α was measured at baseline. RESULTS: Baseline levels of IL-6 were significantly associated with incident lung cancer risk in a model that adjusted for age, gender, race, and site (Model 1) (Hazard RatioT3 vs. T1: 3.34, 95% Confidence Interval: 1.91, 5.85) and in a model adjusted for health factors linked to chronic inflammation (Model 2) (HR T3 vs. T1: 2.57, 95% CI: 1.41, 4.65). The associations observed in time-updated IL-6 (HR T3 vs. T1: 2.47, 95% CI: 1.43, 4.28), cumulatively averaged IL-6 (HR T3 vs. T1: 2.47, 95% CI: 1.43, 4.35), and baseline CRP levels (HR T3 vs. T1: 1.85, 95% CI: 1.11, 3.08) with incident lung cancer in Model 1 were not statistically significant in Model 2. CONCLUSIONS: Baseline CRP and IL-6 levels were associated with increased risk of lung cancer in Model 1 and both models, respectively. Chronic IL-6 inflammation, as quantified by repeated measures was associated with incident lung cancer in Model 1, but not Model 2. Further research is needed to understand the role of CRP and IL-6 in lung carcinogenesis.
OBJECTIVES: We examined the association between three inflammatory markers (Interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α) and incident lung cancer using baseline, updated, and averaged inflammatory measures in older adults. METHODS: We fitted multivariable Cox models to assess whether circulating levels of inflammation markers were associated with incident lung cancers in the Health Aging, Body and Composition (HealthABC) prospective cohort of 3075 older adults aged 70-79 years at baseline. IL-6 and CRP were measured biennially, whereas TNF-α was measured at baseline. RESULTS: Baseline levels of IL-6 were significantly associated with incident lung cancer risk in a model that adjusted for age, gender, race, and site (Model 1) (Hazard RatioT3 vs. T1: 3.34, 95% Confidence Interval: 1.91, 5.85) and in a model adjusted for health factors linked to chronic inflammation (Model 2) (HR T3 vs. T1: 2.57, 95% CI: 1.41, 4.65). The associations observed in time-updated IL-6 (HR T3 vs. T1: 2.47, 95% CI: 1.43, 4.28), cumulatively averaged IL-6 (HR T3 vs. T1: 2.47, 95% CI: 1.43, 4.35), and baseline CRP levels (HR T3 vs. T1: 1.85, 95% CI: 1.11, 3.08) with incident lung cancer in Model 1 were not statistically significant in Model 2. CONCLUSIONS: Baseline CRP and IL-6 levels were associated with increased risk of lung cancer in Model 1 and both models, respectively. Chronic IL-6inflammation, as quantified by repeated measures was associated with incident lung cancer in Model 1, but not Model 2. Further research is needed to understand the role of CRP and IL-6 in lung carcinogenesis.
Authors: Katriina Heikkilä; Ross Harris; Gordon Lowe; Ann Rumley; John Yarnell; John Gallacher; Yoav Ben-Shlomo; Shah Ebrahim; Debbie A Lawlor Journal: Cancer Causes Control Date: 2008-08-15 Impact factor: 2.506
Authors: Meredith S Shiels; Ruth M Pfeiffer; Allan Hildesheim; Eric A Engels; Troy J Kemp; Ju-Hyun Park; Hormuzd A Katki; Jill Koshiol; Gloriana Shelton; Neil E Caporaso; Ligia A Pinto; Anil K Chaturvedi Journal: J Natl Cancer Inst Date: 2013-11-18 Impact factor: 13.506