In the present study, we screened proteomic and cytokine biomarkers between patients with adenomatous polyps and colorectal cancer (CRC) in order to improve our understanding of the molecular mechanisms behind turmorigenesis and tumor progression in CRC. To this end, we performed comparative proteomic analysis of plasma proteins using a combination of 2DE and MS as well as profiled differentially regulated cytokines and chemokines by multiplex bead analysis. Proteomic analysis identified 11 upregulated and 13 downregulated plasma proteins showing significantly different regulation patterns with diagnostic potential for predicting progression from adenoma to carcinoma. Some of these proteins have not previously been implicated in CRC, including upregulated leucine-rich α-2-glycoprotein, hemoglobin subunit β, Ig α-2 chain C region, and complement factor B as well as downregulated afamin, zinc-α-2-glycoprotein, vitronectin, and α-1-antichymotrypsin. In addition, plasma levels of three cytokines/chemokines, including interleukin-8, interferon gamma-induced protein 10, and tumor necrosis factor α, were remarkably elevated in patients with CRC compared to those with adenomatous polyps. Although further clinical validation is required, these proteins and cytokines can be established as novel biomarkers for CRC and/or its progression from colon adenoma.

CD8+ T cells are key factors mediating hepatitis B virus (HBV) clearance. However, these cells are killed through HBV-induced apoptosis during the antigen-presenting period in HBV-induced chronic liver disease (CLD) patients. Interferon-inducible protein 6 (IFI6) delays type I interferon-induced apoptosis in cells. We hypothesized that single nucleotide polymorphisms (SNPs) in the IFI6 could affect the chronicity of CLD. The present study included a discovery stage, in which 195 CLD patients, including chronic hepatitis B (HEP) and cirrhosis patients and 107 spontaneous recovery (SR) controls, were analyzed. The genotype distributions of rs2808426 (C > T) and rs10902662 (C > T) were significantly different between the SR and HEP groups (odds ratio [OR], 6.60; 95% confidence interval [CI], 1.64 to 26.52, p = 0.008 for both SNPs) and between the SR and CLD groups (OR, 4.38; 95% CI, 1.25 to 15.26; p = 0.021 and OR, 4.12; 95% CI, 1.18 to 14.44; p = 0.027, respectively). The distribution of diplotypes that contained these SNPs was significantly different between the SR and HEP groups (OR, 6.58; 95% CI, 1.63 to 25.59; p = 0.008 and OR, 0.15; 95% CI, 0.04 to 0.61; p = 0.008, respectively) and between the SR and CLD groups (OR, 4.38; 95% CI, 1.25 to 15.26; p = 0.021 and OR, 4.12; 95% CI, 1.18 to 14.44; p = 0.027, respectively). We were unable to replicate the association shown by secondary enrolled samples. A large-scale validation study should be performed to confirm the association between IFI6 and HBV clearance.

BackgroundHepatocellular carcinoma (HCC) is one of the most common malignancies occurring worldwide and is most frequent type of liver cancer. The risk for developing HCC increases with the severity of inflammation and fibrosis. The members of the interleukin-1 (IL-1) family are primarily proinflammatory cytokines due to their ability to stimulate the expression of genes associated with inflammation and autoimmune diseases. Several studies have suggested that some proinflammatory cytokines, such as the IL-1 family (IL-1α, IL-1β, and IL-1 receptor antagonist) are involved in the pathogenesis of HCC.Material/MethodsThis study aimed to determine whether polymorphisms in the IL-1 family of genes are associated with HCC. We analyzed 178 HCC patients and 397 controls to investigate the association between polymorphisms in IL-1α, IL-1β, and IL-1 receptor antagonist (IL-1RA) genes and HCC in the Korean population. All subjects were genotyped for the selected SNPs in IL-1α, IL-1β, and IL-1RA genes by Golden-Gate SNP Genotyping Assay.ResultsStatistical analysis revealed a significant association at IL-1β between HCC and controls. Three individual polymorphisms (rs1143633, rs3917356, and rs1143627) were found to be associated with HCC. The SNPs of IL-1β gene (rs1143633A>G and rs1143627T>C) protected against HCC in the dominant model (p=0.027, OR=0.59, 95% CI=0.37–0.94; p=0.019, OR=0.56, 95% CI=0.34–0.91). The SNP of IL-1β gene (rs3917356G>A) increased the risk of HCC in the recessive model (p<0.001, OR=2.58, 95% CI=1.53–4.33), whereas other SNPs in IL-1α and IL-1RA showed no significant association between HCC patients and controls.ConclusionsThese results suggest that IL-1β in the IL-1 family contributes to HCC susceptibility.

BackgroundDietary potassium has negative outcomes in patients with mildly impaired kidney function, while having positive outcomes in patients with hypertension. The association of dietary potassium intake with chronic kidney disease (CKD) development, with presence of hypertension, was studied in the Korean rural population with mildly impaired kidney function.Material/MethodsFrom 3 rural areas of Korea, 5064 participants age ≥40 with CKD stage 2 at baseline were recruited. Patients were classified according to the quartile of dietary potassium intake. Newly developed CKD, defined as estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m2 at the time of follow-up, and eGFR decline, defined as eGFR decrease >15% at follow-up, were studied. The effect of dietary potassium on CKD development and eGFR decline were studied by Cox proportional hazard models. The association of potassium with blood pressures and C-reactive protein was also studied to examine the underlying mechanisms.ResultsCompared to 8.6% in normotensives, 15.7% of hypertensives developed CKD. The hazard ratio (HR) (95% confidence interval) of CKD was lower in high potassium diet only in hypertensives, with 0.60 (0.37–0.99) in the highest quartile. The eGFR decline was also lower in patients with higher potassium diet, with 0.70 (0.50–0.98) in Q3 and 0.54 (0.34–0.85) in Q4. Potassium intake has also been shown to decrease high diastolic blood pressure development (>90 mmHg) in hypertensives at 0.45 (0.25–0.83).ConclusionsDietary potassium was associated with lower risk of CKD development and eGFR decline, and this association was observed only in hypertensives.

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