The association among TP53 rs1042522, pri-miR 34b/c rs4938723 polymorphisms and daily dietary fatty acids in patients with premalignant and malignant oral lesions

Abstract

BackgroundAn important aspect of oral carcinogenesis is individual genetic susceptibility. The two Single Nucleotide Polymorphisms (SNPs) were selected because they are related to different cancers including oral squamous cell carcinoma. AimThe aim of this work was to evaluate the relationship between the daily intake of saturated, monounsaturated, and polyunsaturated fatty acids in people with/without cancer or precancer lesions, and its possible relationship with the TP53 -R72P and pri-miR 34b/c- rs4938723. Subjects and methodsA retrospective study was carried out. The groups of patients were control (n = 27), potentially malignant oral lesions (PPOL) (n = 24), and OSCC (n = 29). Daily dietary data was collected by quantitative-food-frequency questionnaire, and genotyping of SNP was performed using allele-specific PCR or RFLP techniques. The Mann–Whitney-U and logistic regression were applied; setting p < 0.05 for statistical significance. ResultsPatients carrying the GC TP53 rs 1,042,522 were 4 times more likely to develop OSCC in comparison with controls (OR = 4.32; 95% CI [1.23–15.18]; p = 0.0331). Patients with OSCC carried the GC + CC in relation to the GG genotype (OR = 3.84, 95%CI [1.17–12.59]; p = 0.0415) and carrying on the allele T of Pri-miR 34b/c rs4938723 (mutation variant) GC were 3 times more likely to develop OSCC in comparison with subjects with allele C (OR = 3.14, 95% CI [1.08–9.18]; p = 0.0374) (Table 2A). Similar, PPOL patients who have allele T were 8 times more likely to develop the premalignant lesions (OR = 8.22, 95% CI [3.17–21.31]; p = 0.0001). Significant high average values were observed in the intake of saturated (palmitic-stearic-arachidic), monounsaturated (palmitoleic-oleic), and polyunsaturated fatty acids (linoleic-alpha linoleic) mg/day in cases compared to controls. Furthermore, the omega-6/ omega −3 ratio was higher in cases compared to controls. ConclusionHigh-fat dietary intake and the presence of mutant alleles of TP53 and micro34b/c were associated with a high risk of OSCC and PPOL.