Publication: Polymeric immunoglobulin receptor polymorphisms and risk of nasopharyngeal cancer
Issued Date
2003-01-21
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ISSN
14712156
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2-s2.0-0037458093
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Mahidol University
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SCOPUS
Bibliographic Citation
BMC Genetics. Vol.4, (2003)
Suggested Citation
Rungnapa Hirunsatit, Narisorn Kongruttanachok, Kanjana Shotelersuk, Pakpoom Supiyaphun, Narin Voravud, Anavaj Sakuntabhai, Apiwat Mutirangura Polymeric immunoglobulin receptor polymorphisms and risk of nasopharyngeal cancer. BMC Genetics. Vol.4, (2003). doi:10.1186/1471-2156-4-3 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/20772
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Title
Polymeric immunoglobulin receptor polymorphisms and risk of nasopharyngeal cancer
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Abstract
Background: Epstein-Barr virus (EBV) associated nasopharyngeal cancer (NPC) is an important squamous cell cancer endemic in Southeast Asia and the Far East and can be considered a multifactorial genetic disease. This research explores potential associations between nasopharyngeal epithelial EBV receptor and NPC susceptibility. To prove the hypothesis, we evaluated two candidate genes, complement receptor 2 (CR2) and polymeric immunoglobulin receptor (PIGR) by using 4 SNPs, CR2IVS2-848C→T, PIGRIVS3-156G→T, PIGR1093G→A and PIGR1739C→T,to genotype 175 cases and 317 controls, divided into Thai, Chinese and Thai-Chinese based on their respective ethnic origins Results: The results obtained indicated that PIGR is an NPC susceptibility gene. The risk association pertaining to each ethnic group was detected for homozygous PIGR1739C with a significant ethnic group adjusted OR (95%Cl) of 2.71(1.72-4.23) and p < 0.00001. Haplotype of the two missense PIGR SNPs, 1093G→A and 1739C→T, and sequence analyses have confirmed the role of the nucleotide PIGR1739 and excluded possibility of an additional significant nonsynonymous NPC susceptibility SNP. Conclusions: We present genetic evidence leading to hypothesize a possibility of PIGR to function as the EBV nasopharyngeal epithelium receptor via IgA-EBV complex transcytosis failure. The PIGR1739C→T is a missense mutation changing alanine to valine near endoproteolytic cleavage site. This variant could alter the efficiency of PIGR to release IgA-EBV complex and consequently increase the susceptibility of populations in endemic areas to develop NPC. © 2003 Hirusatic et; licensee BioMed Central Ltd.
