The Joint Effect of hOGG1 Single Nucleotide Polymorphism and Betel Quid Chewing on Oral Cancer in Taiwan

• Published in: Anticancer research Vol. 30; no. 10; pp. 4205 - 4208
• Main Authors: TSOU, Yung-An, HUA, Chun-Hung, TSENG, Hsien-Chang, HSU, Chia-Fang, TSAI, Chia-Wen, SUN, Shung-Shung, TSAI, Ru-Yin, TSAI, Ming-Hsui, BAU, Da-Tian
• Format: Journal Article
• Language: English
• Published: Attiki International Institute of Anticancer Research 01.10.2010
• Subjects: Areca - adverse effects; Biological and medical sciences; Chewing; Cocarcinogenesis; Codons; DNA Glycosylases - genetics; Female; Gene polymorphism; Genetic Predisposition to Disease; Hospitals; Humans; Male; Medical sciences; Middle Aged; Mouth Neoplasms - enzymology; Mouth Neoplasms - etiology; Mouth Neoplasms - genetics; Otorhinolaryngology. Stomatology; Polymerase chain reaction; Polymorphism, Single Nucleotide; Restriction fragment length polymorphism; Single-nucleotide polymorphism; Taiwan; Tropical medicine; Tumors; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology; Asia; Taiwan; Human; Genetic variability; Oral cancer; Enzyme; Stomatology; Betel; Genotype; Malignant tumor; Chewing; Epidemiology; Glycosylases; Carcinogen; Cancerology; hOGG1; Risk factor; Genetics; Hydrolases; betel quid; Oral cavity disease; Single nucleotide polymorphism; Public health; Cancer
• ISSN: 0250-7005; 1791-7530

To evaluate the association and interaction among hOGG1 genotypic polymorphism, betel quid chewing status and oral cancer risk in Taiwan. The well-known polymorphic variants of hOGG1, codon 326, were analyzed in association with oral cancer susceptibility, and discussed regarding its joint effect with individual habits on oral cancer susceptibility. In total, 620 patients with oral cancer and 620 healthy controls recruited from the China Medical Hospital were analyzed by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). The hOGG1 codon 326 genotypes were differently distributed between the oral cancer and control groups (p=0.0266) and the C allele of hOGG1 codon 326 was significantly (p=0.0046) more frequently found in cancer patients than in controls. We further analyzed the joint effects of gene variants and habits on oral cancer risk and found an interaction between hOGG1 codon 326 genotype and betel quid chewing status. The association of the C allele for hOGG1 codon 326 with oral cancer risk was found to be significant only in the betel quid chewer group (p=0.0149), not in the non-chewer group (p=0.8028). Our results provide evidence that the C allele of hOGG1 codon 326 may have a joint effect with betel quid chewing on the development of oral cancer.