N-Acetyltransferase 2 gene polymorphism in patients with colorectal carcinoma


Tamer L., Ercan B., Ates N., Degirmenci U., Unlu A., Ates C., ...Daha Fazla

CELL BIOCHEMISTRY AND FUNCTION, cilt.24, ss.131-135, 2006 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 24 Konu: 2
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1002/cbf.1191
  • Dergi Adı: CELL BIOCHEMISTRY AND FUNCTION
  • Sayfa Sayıları: ss.131-135

Özet

The acetylation polymorphism is a common inherited variation in human drug and carcinogen metabolism. Because N-acetyltransferase (NAT2) is important for the detoxification and/or bioactivation of drugs and carcinogens, polymorphisms of this gene have important implications in therapeutics of mid susceptibility to cancer. In this study, NAT2 genotype (NAT2*5A ((CT)-T-481), NAT2*6A (G(590)A), NAT2*7A/B (G(857)A)) and NAT2*14A (G(191)A) and phenotype were determined in 125 patients with colorectal carcinoma and 82 healthy control in Mersin. a city located in the southern region of Turkey. Isolation of the subjects' DNA was performed by using a highly purified PCR template preparation kit/(Roche Diagnostics cat. no: 1796828) and the NAT2 polymorphism was detected using real-time PCR (Roche Diagnostics, GmbH, Mannheim, Germany). According to this study high protein intake is associated with the increased risk for the development of colon cancer (OR = 1.73; 95% CI, 1.10-3.07). Although only NAT2*14A fast type was associated with increased risk in patients with colorectal carcinoma (OR = 3.03; 95% CI, 1.56-5.86), when a high protein diet was considered, NAT2*7A/B fast genotype was also found to be associated with an increased risk (OR = 2.06. 95% CI for NAT2*7A/B. 1.10-3.86; OR = 2.65 95% CI, 1.29-5.46 for NAT2* 14A). Smoking status did not differ between the control and patient groups. Our data suggest that exposure to carcinogens through consumption of a high-protein diet may increase the risk of colorectal carcinoma only in genetically-susceptible individuals. Copyright (c) 2004 John Wiley & Sons, Ltd.