AIM:This study aimed to investigate genotype and allele frequencies of −174 (rs1800795) and −572 (rs1800796) IL-6 promoter gene polymorphisms in Egyptian patients with rheumatoid arthritis (RA) in comparison to control group.METHODS:The study was conducted on 198 Egyptian subjects (99 RA patients and 99 healthy control). The promoter region of the IL-6 gene was amplified by PCR using DNAs from patients and the controls, and their PCR products were digested by suitable enzymes.RESULTS:No statistical differences were found in −572G/C genotype (P = 0.177) or allele (P = 0.147) frequencies between RA patients and controls. Significant differences were observed in −174G/C genotype (P < 0.001) and allele (P < 0.001) frequencies between RA patients and controls.CONCLUSION:A significant association of IL-6 −174G/C gene polymorphism and RA in Egyptian population was found with significantly higher frequencies of GC and CC genotypes and C allele in RA patients compared to controls. No association was found between IL-6 −572G/C gene polymorphism and RA.

It is known that xanthine oxidoreductase contributes significantly to ischemia/reperfusion injury by generating reactive oxygen species. Ischemia-modified albumin (IMA) is a biomarker of acute myocardial ischemia with high sensitivity but moderate specificity. Our study aims to evaluate the xanthine oxidase (XO) system and the IMA level in the serum of patients with ischemic heart disease, and their correlation with traditional cardiac markers. The study was conducted on 60 patients with ischemic heart disease and 22 healthy subjects (control group). Subjects were divided into three groups: group I (30 patients with ST-elevated myocardial infarction), group II (30 patients with chronic stable angina), and the control group (22 subjects). The patients and controls had laboratory tests performed including lipid profile, cardiac enzymes, XO, uric acid, and IMA. The serum levels of XO and IMA were significantly higher in group I (1.65 ± 0.29 U/ml and 0.58 ± 0.15 ABSU, respectively) than in group II (1.11 ± 0.20 U/ml and 0.29 ± 0.10 ABSU, respectively) and the control group (0.95 ± 0.16 U/ml and 0.24 ± 0.08 ABSU, respectively) (P < 0.001). There was a significant positive correlation between XO and IMA in group I. Also, there was significant positive correlation between XO or IMA and other cardiac markers, with the highest level of significance between IMA and creatine kinase (CK-MB). In group II only XO activity was significantly elevated in comparison with controls. These results confirm the role of XO enzyme in ischemic heart disease with involvement of IMA, at a detectable level, during the early necrotic phase.

Breast cancer is the most common invasive cancer in women worldwide. Sirtuin 1 (SIRT1) has recently been shown to have implications in regulating cancer cell growth and apoptosis. SIRT1 regulates Forkhead box O3a (FOXO3a) by both inhibiting FOXO3-induced apoptosis and potentiating the ability of FOXO3a to resist oxidative stress. Matrix metalloproteinase 2 (MMP2) participates in tumor invasion and metastasis by degrading extracellular matrix. SIRT1 up regulates MMP2 expression by its deacetylation activity. This study aimed to investigate the expression of SIRT1, FOXO3a and MMP2 in breast tissues of women with breast cancer. In addition, the effect of SIRT1 inhibition on both FOXO3a and MMP2 expression in breast cancer (MCF-7) cells was assessed. The expression levels of SIRT1, FOXO3a and MMP2 in the breast tissues were determined by real-time PCR in 60 patients with malignant tumor and in 24 patients with benign tumors. After SIRT1 inhibition, protein levels of SIRT1 and FOXO3a were assessed by Western Blot and levels of MMP2 by ELISA in MCF-7 cells. The expression levels of SIRT1, FOXO3a and MMP2 were significantly higher in breast cancer tissues compared to in benign breast tumor and adjacent normal tissues. SIRT1, MMP2 and FOXO3a expression were associated directly with each other. SIRT1 inhibition suppresses MMP2 and FOXO3a expression compared to control MCF7. Sirtinol (SIRT1 inhibitor) effectively induced inhibition of MMP2 and FOXO3a expression in MCF-7 cells, indicating the promising therapeutic strategy of targeting SIRT1 for breast cancer.

The third most common cancer-related cause of death worldwide is hepatocellular carcinoma (HCC). and it is the sixth most common primary malignancy overall. Egypt had the hepatitis C virus's highest prevalence (HCV). A critical topic of study is the association between HCV and HCC. PR domain zinc finger protein 1 (PRDM1) functions as a tumor suppressor in B and T cells and is critical for plasma cell development and the exhaustion of T lymphocytes caused by cancer and chronic viral infections. Aim: This study aimed to compare Egyptian patients with HCC to a control group to determine the allele frequencies and genotype of the rs1010273 PRDM1 gene polymorphism. Methods: Included 200 Egyptian patients (100 HCC and 100 control). All participants underwent laboratory evaluations, comprising hepatitis markers (HBsAg, anti-HCV-Ab), liver function tests, serum alpha-fetoprotein, and complete blood count. Using the TaqMan allelic discrimination assay method, the PRDM1 rs1010273 was genotyped. Results: Unlike the healthy controls, the HCC patients had a greater frequency of the GA genotype (43% vs. 20%) and the A allele (26.5% vs. 10%). A significant difference was found between the GA and A allele of PRDM1genotype of HCC patients and controls (P<.001). Conclusions: A statistically significant and greater frequency of the A allele and GA genotype was found in HCC patients compared to controls, indicating a relationship between the PRDM1 AA+GA gene polymorphism and the HCC Egyptian population. The A allele was assumed to be a risk factor for HCC (OR=11.212). SNP (rs1010273G/A) may be an optional valuable marker.