scholarly journals Polymorphisms of Tumor Necrosis Factor Alpha in Moroccan Patients with Gastric Pathology: New Single-Nucleotide Polymorphisms in TNF-α−193(G/A)

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
A. Essadik ◽  
H. Jouhadi ◽  
T. Rhouda ◽  
S. Nadifiyine ◽  
A. Kettani ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
High Risk ◽  
Tumor Necrosis Factor ◽  
Promoter Region ◽  
Tumor Necrosis ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Factor Alpha ◽  
Necrosis Factor

Polymorphisms in tumor necrosis factor alpha (TNF-α) gene are emerging as key determinants of gastric diseases. The TNF-α−308(G/A) and TNF-α−238(G/A) single-nucleotide polymorphisms SNPs are the most extensively studied. However, all these studies are conducted in Caucasian and Asian populations. Thus, for the first time in Africa, we sought to investigate whether polymorphisms in TNF-αgene were associated with the development of gastric pathology in Morocco. Two SNPs located in the promoter region (positions −308 and −238) in TNF-αgene were genotyped in 244 individuals (170 patients and 74 healthy controls). Odds ratios (ORs) and 95% confidence intervals (CI) were estimated using logistic regression analysis. The TNF-α−238(G/A) genotype was significantly associated with a high risk of gastritis and gastric cancer (GC) (P=0.001andP=0.002, resp.). Furthermore, a new polymorphism located in the promoter region at position −193 in TNF-αgene was identified. The distribution of this SNP was markedly different in patients suffering from ulcers. The association between TNF-α−193(G/A) genotype and high risk of ulcer was significant (P=0.03). These results suggest that the TNF-α−193(G/A) allele has a protective function against gastric cancer by developing ulcer.

scholarly journals Tumor Necrosis Factor Alpha-863 C/A Single Nucleotide Polymorphisms and Nephrotic Syndrome

2020 ◽  
Vol 10 (03) ◽  
pp. 319-322
Author(s):  
Ahmed Abdul-Hassan Abbas ◽  
Zainab J. Fadhil ◽  
Shatha Hussein Ali
Keyword(s):  
Nephrotic Syndrome ◽  
Tumor Necrosis Factor ◽  
Serum Level ◽  
Tumor Necrosis ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Introduction: Cytokines act as a mediator of inflammation in childhood nephrotic syndrome. Polymorphisms of cytokines genes may influence susceptibility to nephrotic syndrome (NS), as well as, patients’ steroid responses. Objective: To study the association of tumor necrosis factor-alpha single nucleotide polymorphisms (TNF-α SNP) (-863 C/A) with the development of NS in addition to access to their effects on serum level of TNF and the response to steroid therapy. Patients and Methods: This study included 60 patients (19 female and 41 male) with nephrotic syndrome; their ages ranged from 2 to 18 years. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to assess the TNF-α gene polymorphism. Results: According to the digestion pattern of RFLP-PCR products of TNF-α-863, this polymorphism had three genotypes, which were CC, CA, and AA, in both NS patients and controls. Also, the current result observed that -863 SNP do not affect the serum level of TNF-α and steroid responsiveness in patients with nephrotic syndrome. Conclusion: This polymorphism did not show any significant association with response to steroid therapy and TNF serum level neither at genotype nor at allele level.

scholarly journals The core promoter region of the tumor necrosis factor alpha gene confers phorbol ester responsiveness to upstream transcriptional activators.

1992 ◽  
Vol 12 (3) ◽  
pp. 1352-1356 ◽  
Author(s):  
D C Leitman ◽  
E R Mackow ◽  
T Williams ◽  
J D Baxter ◽  
B L West
Keyword(s):  
Transcription Factors ◽  
Tumor Necrosis Factor ◽  
Promoter Region ◽  
Tumor Necrosis ◽  
Core Promoter ◽  
Core Promoter Region ◽  
Necrosis Factor Alpha ◽  
The Core ◽  
Factor Alpha ◽  
Necrosis Factor

Activators of protein kinase C, such as 12-O-tetradecanoylphorbol 13-acetate (TPA), are known to regulate the expression of many genes, including the tumor necrosis factor alpha (TNF) gene, by affecting the level or activity of upstream transcription factors. To investigate the mechanism whereby TPA activates the TNF promoter, a series of 5'-deletion mutants of the human TNF promoter linked to chloramphenicol acetyltransferase was transfected into U937 human promonocytic cells. TPA produced a 7- to 11-fold activation of all TNF promoters tested, even those promoters truncated to contain only the core promoter with no upstream enhancer elements. The proximal TNF promoter containing only 28 nucleotides upstream and 10 nucleotides downstream of the RNA start site confers TPA activation to a variety of unrelated upstream enhancer elements and transcription factors, including Sp1, CTF/NF1, cyclic AMP-response element, GAL-E1a, and GAL-VP16. The level of activation by TPA depends on the TATA box structure, since the TPA response is greater in promoters containing the sequence TATAAA than in those containing TATTAA or TATTTA. These findings suggest that the core promoter region is a target for gene regulation by second-messenger pathways.

Tumor necrosis factor-alpha single nucleotide polymorphisms in juvenile systemic lupus erythematosus

2015 ◽  
Vol 76 (8) ◽  
pp. 533-536 ◽  
Author(s):  
Fatemeh Tahghighi ◽  
Vahid Ziaee ◽  
Mohammad Hassan Moradinejad ◽  
Arezou Rezaei ◽  
Sara Harsini ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Nucleotide Polymorphisms ◽  
Systemic Lupus ◽  
Juvenile Systemic Lupus Erythematosus ◽  
Necrosis Factor Alpha ◽  
Single Nucleotide ◽  
Factor Alpha ◽  
Necrosis Factor
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