TAP1 gene polymorphisms and nasopharyngeal carcinoma risk in a Tunisian population

• Published in: Cancer genetics and cytogenetics Vol. 175; no. 1; pp. 41 - 46
• Main Authors: Hassen, Elham, Farhat, Karim, Gabbouj, Sallouha, Jalbout, Majida, Bouaouina, Noureddine, Chouchane, Lotfi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2007
• Subjects: Adolescent; Adult; Aged; Alleles; ATP-Binding Cassette Sub-Family B Member 2; ATP-Binding Cassette Transporters - genetics; Child; Female; Gene Frequency; Genotype; Hematology, Oncology and Palliative Medicine; Humans; Linkage Disequilibrium; Male; Medical Education; Middle Aged; Nasopharyngeal Neoplasms - epidemiology; Nasopharyngeal Neoplasms - genetics; Nasopharyngeal Neoplasms - pathology; Odds Ratio; Polymorphism, Genetic; Tunisia - epidemiology
• ISSN: 0165-4608; 1873-4456
• DOI: 10.1016/j.cancergencyto.2007.01.009

To find out whether polymorphisms 333-Ile/Val and 637-Asp/Gly of the transporter part of the antigen processing 1 gene ( TAP1) are associated with the development of nasopharyngeal carcinoma (NPC), we studied a total of 374 subjects (209 patients and 165 controls). We used the amplification refractory mutation system polymerase chain reaction (ARMS-PCR) method for analyzing the TAP1 gene polymorphisms. We found a significant difference between the patients and the controls in both the TAP1 codon 333 and codon 637 ( P = 0.009 and P = 0.002, respectively). We also found that genotypes with the A allele were present in 206 patients with NPC and 155 controls (98.5 vs. 93.9%; P = 0.032; OR = 4.43) and that genotypes with the B allele were more often present in the control group (45 vs. 32%; P = 0.004; OR = 0.48), suggesting a significant positive association of the A allele with NPC risk and a protective role of the B allele. We have observed an association between the distribution of TAP1 alleles and the NPC patient's age at onset, compared with controls. These results back up the fact that the etiology of NPC in intermediate-risk countries is completely different in each peak of age prevalence and that each peak may possess its own particular oncogenic mechanism.