Correlation of p21 gene codon 31 polymorphism and TNF-α gene polymorphism with nasopharyngeal carcinoma

✍ Scribed by Ming-Hsui Tsai; Wen-Chi Chen; Fuu-Jen Tsai

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 48 KB
• Volume: 16
• Category: Article
• ISSN: 0887-8013
• DOI: 10.1002/jcla.10032

✦ Synopsis

Abstract

Background p21 (WAF1/CIP1) is a downstream protein from p53 and can arrest the cell cycle at the G1/S phase in response to signal from p53. The most frequently seen polymorphic site is at codon 31, where a base change from AGC to AGA causes an amino acid change from serine to arginine. Tumor necrosis factor‐alpha (TNF‐α) is a cytokine that is secreted from macrophages, and is related to a sequence of events in the response to inflammation and cancer formation. The TNF‐α gene promoter –308 G/A polymorphism has been reported to be associated with some cancers. In this study, these polymorphisms were proposed to be a candidate genetic marker of nasopharyngeal carcinoma (NPC). The distribution was analyzed in 47 NPC patients and a control group of 119 healthy people. The association of the p21 codon 31 polymorphism with NPC was detected by polymerase chain reaction (PCR) and restriction analysis by Blp I endonuclease, and calculated by the chi‐square test. The TNF‐α gene promoter –308 G/A polymorphism was identified by Nco I endonuclease. The distribution of the gene p21 codon 31 polymorphisms showed no significant difference between the two groups. The serine form of p21 codon 31 was more prominent in smokers than nonsmokers among the NPC patients (P < 0.05). There was no significant difference in the distribution of TNF‐α gene promoter –308 G/A polymorphism between control and cancer patients. The results indicate that the gene p21 codon 31 polymorphism and TNF‐α promoter –308 polymorphism are not correlated with NPC. However, the difference between smokers and nonsmokers suggests that an environmental factor may be involved in association with the p21 gene in the formation of NPC. J. Clin. Lab. Anal. 16:146–150, 2002. © 2002 Wiley‐Liss, Inc.