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Cancer Causes Control. 2015 Oct;26(10):1449-60. doi: 10.1007/s10552-015-0641-1. Epub 2015 Jul 29.

Interleukin-6 and risk of colorectal cancer: results from the CLUE II cohort and a meta-analysis of prospective studies.

Author information

1
Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Stavros Niarchos Av., University Campus, Ioannina, Greece.
2
Division of Epidemiology, University of Texas School of Public Health, Houston, TX, USA.
3
Division of Urology, University of Texas Medical School, Houston, TX, USA.
4
George W. Comstock Center for Public Health Research and Prevention, Johns Hopkins Bloomberg School of Public Health, Hagerstown, MD, USA.
5
Department of Laboratory Medicine, Harvard Medical School and Children's Hospital, Boston, MA, USA.
6
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
7
Department of Urology and James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
8
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA.
9
Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Stavros Niarchos Av., University Campus, Ioannina, Greece. ktsilidi@cc.uoi.gr.
10
Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. ktsilidi@cc.uoi.gr.

Abstract

PURPOSE:

The association between prediagnostic interleukin-6 (IL-6) concentrations and risk of colorectal cancer was evaluated in a nested case-control study and a meta-analysis of prospective studies.

METHODS:

Colorectal cancer cases (n = 173) and matched controls (n = 345) were identified between 1989 and 2000 among participants in the CLUE II cohort of Washington Country, Maryland. Matched odds ratios and the corresponding 95 % confidence intervals (CIs) were estimated using conditional logistic regression models.

RESULTS:

Participants in the highest third of plasma IL-6 concentration had a 2.48 times higher risk of colon cancer compared to participants in the bottom third (95 % CI 1.26-4.87; p-trend 0.02) after multivariate adjustment. This association did not differ according to the stage of disease, age, sex, or other potential modifying variables and remained statistically significant after adjustment for C-reactive protein concentrations. No statistically significant association was observed for rectal cancer risk. The meta-analysis of six prospective studies yielded an increased but borderline statistically significant risk of colon cancer per 1 U increase in naturally logarithm-transformed IL-6 (summary RR 1.22; 95 % CI 1.00-1.49; I (2) 46 %). An inverse association was noted for rectal cancer (RR 0.69; 95 % CI 0.54-0.88; I (2) 0 %), but there was evidence for small-study effects (p 0.02).

CONCLUSION:

Our findings provide support for a modest positive association between IL-6 concentrations and colon cancer risk. More work is needed to determine whether IL-6 is a valid marker of colorectal inflammation and whether such inflammation contributes to colon and rectal cancer risk.

KEYWORDS:

Cohort study; Colorectal cancer; Inflammation; Meta-analysis

PMID:
26220152
PMCID:
PMC4763881
DOI:
10.1007/s10552-015-0641-1
[Indexed for MEDLINE]
Free PMC Article

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