Association of dipeptidyl peptidase IV polymorphism with clinicopathological characters of oral cancer

<jats:title>Abstract</jats:title><jats:sec><jats:title>Objective</jats:title><jats:p>To evaluate the associations between dipeptidyl peptidase IV (<jats:italic>DPP4</jats:italic>) single‐nucleotide polymorphism (SNP) and clinicopathological characteristics of oral cancer.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Four loci of <jats:italic>DPP4</jats:italic> SNPs (rs7608798 A/G, rs3788979 C/T, rs2268889 T/C, and rs6741949 G/C) were genotyped by using the TaqMan allelic discrimination in 1238 oral cancers patients and 1197 non‐cancer individuals.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>The percentage of <jats:italic>DPP4</jats:italic> SNP rs2268889 TC + CC was significantly higher in the oral cancer participants compared to the control group (odds ratio [OR]: 1.178, 95% confidence interval (CI): 1.004–1.382, <jats:italic>p</jats:italic> = 0.045). Among 1676 smokers, <jats:italic>DPP4</jats:italic> polymorphisms carriers with betel quid chewing were found to have an 8.785‐ to 10.903‐fold risk to have oral cancer compared to <jats:italic>DPP4</jats:italic> wild‐type carriers without betel quid chewing. Similar trend was found in individuals with alcohol consumption. Moreover, the oral cancer individuals without cigarette smoking history with at least one varied C allele of <jats:italic>DPP4</jats:italic> rs2268889 had a significantly higher percentage of large tumor size with the wild‐type TT homozygote (<jats:italic>p</jats:italic> = 0.011).</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>The <jats:italic>DPP4</jats:italic> SNP may correlate to the development of oral cancer in those with cigarette smoking and alcohol consumption. Besides, the <jats:italic>DPP4</jats:italic> SNP rs2268889 could relate to worse clinical course of oral cancer in non‐smokers.</jats:p></jats:sec>