Effect of CC chemokine ligand 5 and CC chemokine receptor 5 genes polymorphisms on the risk and clinicopathological development of oral cancer

Chia Jui Weng, Ming Hsien Chien, Chiao Wen Lin, Tsung Te Chung, Athanasios I. Zavras, Chiung Man Tsai, Mu Kuan Chen, Shun Fa Yang

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Inflammation can be induced by cytokines, chemokines, and their receptors, and it is believed to be a risk factor on tumor initiation and progression. The contribution of CC chemokine ligand 5 (CCL5) and CC chemokine receptor 5 (CCR5) on the risk and prognosis of oral cancer is still poorly investigated. The aims of this study were to investigate the impacts of single nucleotide polymorphisms (SNPs) in CCL5 and CCR5 genes and the synergistic effects of these SNPs on the risk and clinicopathological characteristics of oral cancer. In this case-control study, a total of 253 oral cancer patients and 347 controls were recruited. The genetic polymorphisms of CCL5-28, -403 and CCR5-59029 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyping analysis. The results of statistical analysis showed that the subjects with CCL5-28 CG, CCL5-28 CG or GG, and CCL5-403 TT polymorphic genotype as well as the subjects with the combinations of CCL5-28 CG/-403 CT and CCL5-28 CG/-403 TT genotypes having a significant higher risk to oral cancer than those with wild-type genotypes. Moreover, the oral cancer patients with the combination of CCL5-28 CG/-403 TT genotype presented a lower risk for developing a moderately or poorly differentiated status as compared to those with the combination of CCL5-28 CC/-403 CC genotype. These results suggest that the SNPs in CCL5-28 and -403 genes could increase the risk to have oral cancer, and the combinative effect of CCL5-28 CG and -403 TT genes might also increase the oral cancer risk but reduce the clinicopathological development of oral cancer patients.

Original languageEnglish
Pages (from-to)767-772
Number of pages6
JournalOral Oncology
Volume46
Issue number10
DOIs
Publication statusPublished - Oct 2010

Fingerprint

CCR5 Receptors
CC Chemokines
Mouth Neoplasms
Ligands
Genes
Genotype
Single Nucleotide Polymorphism
Chemokine Receptors
Genetic Polymorphisms
Restriction Fragment Length Polymorphisms

Keywords

  • CC chemokine ligand 5
  • CC chemokine receptor 5
  • Oral cancer
  • Single nucleotide polymorphism

ASJC Scopus subject areas

  • Oncology
  • Oral Surgery
  • Cancer Research

Cite this

Effect of CC chemokine ligand 5 and CC chemokine receptor 5 genes polymorphisms on the risk and clinicopathological development of oral cancer. / Weng, Chia Jui; Chien, Ming Hsien; Lin, Chiao Wen; Chung, Tsung Te; Zavras, Athanasios I.; Tsai, Chiung Man; Chen, Mu Kuan; Yang, Shun Fa.

In: Oral Oncology, Vol. 46, No. 10, 10.2010, p. 767-772.

Research output: Contribution to journalArticle

Weng, Chia Jui ; Chien, Ming Hsien ; Lin, Chiao Wen ; Chung, Tsung Te ; Zavras, Athanasios I. ; Tsai, Chiung Man ; Chen, Mu Kuan ; Yang, Shun Fa. / Effect of CC chemokine ligand 5 and CC chemokine receptor 5 genes polymorphisms on the risk and clinicopathological development of oral cancer. In: Oral Oncology. 2010 ; Vol. 46, No. 10. pp. 767-772.
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abstract = "Inflammation can be induced by cytokines, chemokines, and their receptors, and it is believed to be a risk factor on tumor initiation and progression. The contribution of CC chemokine ligand 5 (CCL5) and CC chemokine receptor 5 (CCR5) on the risk and prognosis of oral cancer is still poorly investigated. The aims of this study were to investigate the impacts of single nucleotide polymorphisms (SNPs) in CCL5 and CCR5 genes and the synergistic effects of these SNPs on the risk and clinicopathological characteristics of oral cancer. In this case-control study, a total of 253 oral cancer patients and 347 controls were recruited. The genetic polymorphisms of CCL5-28, -403 and CCR5-59029 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyping analysis. The results of statistical analysis showed that the subjects with CCL5-28 CG, CCL5-28 CG or GG, and CCL5-403 TT polymorphic genotype as well as the subjects with the combinations of CCL5-28 CG/-403 CT and CCL5-28 CG/-403 TT genotypes having a significant higher risk to oral cancer than those with wild-type genotypes. Moreover, the oral cancer patients with the combination of CCL5-28 CG/-403 TT genotype presented a lower risk for developing a moderately or poorly differentiated status as compared to those with the combination of CCL5-28 CC/-403 CC genotype. These results suggest that the SNPs in CCL5-28 and -403 genes could increase the risk to have oral cancer, and the combinative effect of CCL5-28 CG and -403 TT genes might also increase the oral cancer risk but reduce the clinicopathological development of oral cancer patients.",
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AB - Inflammation can be induced by cytokines, chemokines, and their receptors, and it is believed to be a risk factor on tumor initiation and progression. The contribution of CC chemokine ligand 5 (CCL5) and CC chemokine receptor 5 (CCR5) on the risk and prognosis of oral cancer is still poorly investigated. The aims of this study were to investigate the impacts of single nucleotide polymorphisms (SNPs) in CCL5 and CCR5 genes and the synergistic effects of these SNPs on the risk and clinicopathological characteristics of oral cancer. In this case-control study, a total of 253 oral cancer patients and 347 controls were recruited. The genetic polymorphisms of CCL5-28, -403 and CCR5-59029 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) genotyping analysis. The results of statistical analysis showed that the subjects with CCL5-28 CG, CCL5-28 CG or GG, and CCL5-403 TT polymorphic genotype as well as the subjects with the combinations of CCL5-28 CG/-403 CT and CCL5-28 CG/-403 TT genotypes having a significant higher risk to oral cancer than those with wild-type genotypes. Moreover, the oral cancer patients with the combination of CCL5-28 CG/-403 TT genotype presented a lower risk for developing a moderately or poorly differentiated status as compared to those with the combination of CCL5-28 CC/-403 CC genotype. These results suggest that the SNPs in CCL5-28 and -403 genes could increase the risk to have oral cancer, and the combinative effect of CCL5-28 CG and -403 TT genes might also increase the oral cancer risk but reduce the clinicopathological development of oral cancer patients.

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