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sTRAIL Serum Levels and TRAIL 1595 Genotypes: Associations with Progress and Prognosis of Colorectal Carcinoma

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DOI: 10.4236/jct.2012.326120    3,368 Downloads   5,622 Views   Citations

ABSTRACT

Programmed cell death called apoptosis, plays an important role in the development and maintenance of tissue homeostasis and abnormalities in apoptotic function have been known as important events in the pathogenesis of many cancer types, such as colorectal cancer. It has been shown that both the membrane-bound TRAIL and sTRAIL can induce apoptosis in several tumor types by activating death receptors. Our study was to investigate the existence of TRAIL 1595 C/T SNP in colorectal cancer patients and possible effects of this substitution on serum levels of sTRAIL. In the present study, TRAIL 1595 C/T polymorphism was genotyped in 76 patients with colorectal cancer and 98 healthy subjects using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. There were no significant differences in the distribution of TRAIL 1595 C/T genotypes and frequencies of the alleles between colorectal cancer patients and controls. The increased frequency of TRAIL 1595 homozygotes genotypes in patients who had advanced tumour stage was statistically significant (p = 0.0082). Serum sTRAIL levels in the colorectal patients with CT genotype were lower than those of patients with early tumor stage (p = 0.028). The decreased sTRAIL levels were observed in the patients with distant metastasis and CT genotype (p = 0.023). Our findings have suggested that TRAIL 1595 C/T genotypes and sTRAIL levels might be associated with the progression of colorectal cancer in Turkish population.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

İ. Yaylım, N. Ozkan, S. Turan, G. Korkmaz, Y. Yıldız, C. Cacina, B. Toptaş and S. Arıkan, "sTRAIL Serum Levels and TRAIL 1595 Genotypes: Associations with Progress and Prognosis of Colorectal Carcinoma," Journal of Cancer Therapy, Vol. 3 No. 6A, 2012, pp. 941-947. doi: 10.4236/jct.2012.326120.

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