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1.
EJB-Egyptian Journal of Biochemistry and Molecular Biology [The]. 2015; 33 (1-2): 16-33
in English | IMEMR | ID: emr-177528

ABSTRACT

Cancer is one the most concerning complication of longstanding ulcerative colitis [UC]. This study was undertaken to investigate the possible association between eNOS gene intron 4 polymorphism and the development of UC-associated colorectal cancer. It was carried out on 120 subjects; distributed as follows: 40 patients with UC associated colorectal cancer, 40 patients with UC who did not develop colorectal cancer and 40 control subjects. Genotypes [aa, bb, ab] for eNOS gene intron 4 polymorphism were identified using amplified fragment length polymorphism PCR. Plasma nitrate and nitrite levels were used to estimate the amounts of endogenous nitric oxide formation using nitric oxide colorimetric assay kit. Our preliminary data revealed that, compared to the bb genotype, the aa and ab eNOS genotypes were significantly associated with increased risk of developing UC associated colorectal cancer. Meanwhile, in UC associated - colorectal cancer and UC patients groups, plasma NO levels were higher in patients with 4a4a/4a4b genotypes compared to those with bb genotype. It can be concluded from our preliminary study that a allele variant of eNOS intron 4 polymorphism may be associated with increased risk of development of UC associated colorectal cancer, however, large scaled studies are needed to verify these preliminary results


Subject(s)
Humans , Female , Male , Middle Aged , Polymorphism, Genetic , Introns , Colitis, Ulcerative , Colorectal Neoplasms
2.
EJB-Egyptian Journal of Biochemistry and Molecular Biology [The]. 2014; 32 (2): 154-171
in English | IMEMR | ID: emr-162404

ABSTRACT

Tumor necrosis factor -like weak inducer of apoptosis [TWEAK] triggers multiple cellular activities in a wide variety of cells, ranging from proliferation to cell death. It also causes upregulation of chemokine [C-X-C motif] receptor 5, and its ligand, chemokine [C-XC motif] ligand 13 [CXCL13]. However, the precise roles of TWEAK and CXCL13 in the pathogenesis of SLE and their association with disease activity still obscure. The study included forty SLE patients and twenty control subjects. SLE disease activity was evaluated by Systemic Lupus Erythematosus Disease Activity Index [SLEDAI] 2000 score. Anti-dsDNA antibodies, serum complement C3, high sensitivity CRP [hsCRP] concentrations, TWEAK and CXCL 13 serum concentrations were detected by ELISA. TWEAK mRNA expression in peripheral blood mononuclear cells was estimated by relative quantitative Real Time-PCR. Serum concentrations of TWEAK and CXCL13 were significantly elevated in SLE patients compared to controls [p < 0.05] with significant increase in patients with active SLE compared to those with inactive disease [p< 0.05], they also significantly correlated with SLEDAI score and anti-dsDNA antibodies. TWEAK mRNA levels increased significantly in active lupus compared to inactive disease. It can be concluded that TWEAK serum and expression levels together with its inducible chemokine CXCL13 serum levels may benefit as biomarkers for prediction of SLE disease activity, as well as possible targets for personalized therapies due to their involvement in the pathogenesis of SLE

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