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Circulating Inflammation Proteins Associated With Lung Cancer in African Americans
Authors:Claire L. Meaney  Khadijah A. Mitchell  Adriana Zingone  Derek Brown  Elise Bowman  Yunkai Yu  Angela S. Wenzlaff  Christine Neslund-Dudas  Sharon R. Pine  Liang Cao  Ann G. Schwartz  Bríd M. Ryan
Affiliation:1. Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland;2. Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland;3. Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan;4. Henry Ford Health System, Detroit, Michigan;5. Department of Medicine, Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey
Abstract:IntroductionLung cancer incidence is higher among African Americans (AAs) compared with European Americans (EAs) in the United States. We and others have previously shown a relationship between immune and inflammation proteins with lung cancer in EAs. Our aim was to investigate the etiologic relationship between inflammation and lung cancer in AAs.MethodsWe adopted a two-stage, independent study design (discovery cases, n = 316; control cases, n = 509) (validation cases, n = 399; control cases, n = 400 controls) and measured 30 inflammation proteins in blood using Meso Scale Discovery V- PLEX multiplex assays.ResultsWe identified and validated 10 proteins associated with lung cancer in AAS, some that were common between EAs and AAs (C-reactive proteins [OR: 2.90; 95% confidence interval (CI): 1.99–4.22], interferon γ [OR: 1.55; 95% CI: 1.10–2.19], interleukin 6 [OR: 6.28; 95% CI: 4.10–9.63], interleukin 8 [OR: 2.76; 95% CI: 1.92–3.98]) and some that are only observed among AAs (interleukin 10 [OR: 1.69; 95% CI: 1.20–2.38], interleukin 15 [OR: 2.83; 95% CI: 1.96–4.07], interferon gamma-induced protein 10 [OR: 1.54; 95% CI: 1.09–2.18], monocyte chemotactic protein-4 [OR: 0.54; 95% CI: 0.38–0.76], macrophage inflammatory protein-1 alpha [OR: 1.57; 95% CI: 1.12–2.21], and tumor necrosis factor β [OR: 0.52; 95% CI: 0.37–0.74]). We did not find evidence that either menthol cigarette smoking or global genetic ancestry drove these population differences.ConclusionsOur results highlight a distinct inflammation profile associated with lung cancer in AAs compared with EAs. These data provide new insight into the etiology of lung cancer in AAs. Further work is needed to understand what drives this relationship with lung cancer and whether these proteins have utility in the setting of early diagnosis.
Keywords:Corresponding author. Address for correspondence: Bríd M. Ryan   PhD   MPH   Laboratory of Human Carcinogenesis   Center for Cancer Research   National Cancer Institute   37 Convent Drive   Room 3060C Bethesda   MD 20892.
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