Chronic inflammation is implicated in the development of colorectal cancer, and the plasma inflammatory biomarker macrophage inhibitory cytokine-1 (MIC-1, GDF15) may have a direct role in tumorigenesis.
As reported in Journal of the National Cancer Institute, Mehta and colleagues found that subjects in the highest (5th) quintile of plasma MIC-1 as measured by enzyme-linked immunosorbent assay had significantly increased risk of colorectal cancer (relative risk [RR] = 1.93, P = .004 for trend) compared with the lowest quintile on multivariate analysis in a nested case-control study.
Further, for patients in the four highest MIC-1 quintiles, regular use vs nonuse of aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with significantly reduced risk of prostaglandin-endoperoxide synthase 2 (PTGS2)/cyclooxygenase-2 (COX-2)–positive colorectal cancer (RR = 0.60, 95% confidence interval [CI] = 0.41– 0.88) but not PTGS2-negative colorectal cancer (RR = 1.21, 95% CI = 0.71–2.07).
Aspirin and NSAID use was not associated with a significantly altered risk of PTGS2-positive colorectal cancer (RR = 0.57, 95% CI = 0.21–1.54) or PTGS2-negative colorectal cancer (RR = 1.41, 95% CI = 0.47–4.23) in patients in the lowest MIC-1 quintile.
The investigators concluded, “Our results support an association between higher levels of circulating MIC-1 (GDF15) and [colorectal cancer]. Aspirin/NSAID use appeared to lower risk of PTGS2-positive cancers, particularly among individuals with high levels of circulating MIC-1.” ■
Mehta RS, et al: J Natl Cancer Inst 106(4):dju016, 2014.