|
Publication
|
Title of Article |
Polymorphism of interleukin-6 receptor is associated with cholangiocarcinoma risk |
Date of Acceptance |
18 June 2014 |
Journal |
Title of Journal |
Asian Pacific Journal of Cancer Prevention (APJCP) |
Standard |
SCOPUS |
Institute of Journal |
UICC-Asia Regional Office/APOCP Coordination |
ISBN/ISSN |
|
Volume |
15 |
Issue |
14 |
Month |
|
Year of Publication |
2014 |
Page |
|
Abstract |
The cholangiocarcinoma (CCA) is a relatively rare cancer worldwide but it is highly prevalent in Thailand where the liver fluke, Opisthorchis viverriniis endemic. There are reports that interleukin 6 (IL-6) may play an important role in the pathogenesis of opisthorchiasis associated CCA. Functionally, IL-6 can act on target cells through its receptor, IL-6R, and IL-6R polymorphisms may affect the functional activity of IL-6 leading to susceptibility to cholangiocarcinogenesis. Therefore, we assessed the association of the 48892 A/C (Asp358Ala) polymorphism in exon 9 of the IL-6R gene in 79 CCA cases compared to 80 healthy controls using the PCR-RFLP technique. The results showed significant differences between CCA cases and controls in overall genotype (p=0.001) and allele frequencies (p=0.0002). Chi-square for trend test revealed a significant association between genotype and CCA susceptibility (p=0.0002). The odds ratios (ORs) for genotype were 0.283 (95% CI=0.131-0.605, AC vs. AA; p=0.0003) and 0.206 (95% CI=0.196-1.245, CC vs. AA; p=0.0416), the OR for alleles was 0.347 (95% CI=0.187-0.633, allele C vs. allele A; p=0.0002) and that for the carrier C variant was 0.272 (95% CI=0.130-0.564; p=0.0001). This study demonstrated a close association between an IL-6R polymorphism, specifically higher A allele, and cholangiocarcinoma. |
Keyword |
Interleukin 6 receptor, Polymorphism, Cholangiocarcinoma, opisthorchiasis, PCR-RFL |
Author |
|
Reviewing Status |
มีผู้ประเมินอิสระ |
Status |
ได้รับการตอบรับให้ตีพิมพ์ |
Level of Publication |
นานาชาติ |
citation |
true |
Part of thesis |
true |
Attach file |
|
Citation |
0
|
|
|
|
|
|
|