The variant of pri-mir-26a-1 polymorphism is associated with decreased risk of betel quid-related oral premalignant lesions and oral squamous cell carcinoma

Oral Surg Oral Med Oral Pathol Oral Radiol. 2017 Oct;124(4):378-389.e1. doi: 10.1016/j.oooo.2017.05.515. Epub 2017 Jun 8.

Abstract

Objectives: This case-control study evaluated the association of the single nucleotide polymorphism rs7372209 (T>C) in pri-mir-26a-1 with the risk and progression of betel quid (BQ)-related oral premalignant lesions (OPLs) and oral squamous cell carcinoma (OSCC).

Study design: In total, 597 BQ chewers were recruited: 196 healthy controls, 241 patients with OPLs, and 160 patients with OSCC. Genotypes were determined using the TaqMan real-time assay.

Results: The C/T + T/T genotypes and T allele in pri-mir-26a-1 were correlated with a decreased risk of BQ-related OPLs (P = .038 and .005, respectively), oral leukoplakia (P = .01 and .001, respectively), and advanced-stage OSCC (P = .021 and .004, respectively). The effects of the C/T + T/T genotypes and T allele on the decreased risk of OPLs were potent in the older age group (both Pinteraction < .001), heavy smokers (Pinteraction ≤ .003 and .006, respectively) and alcohol drinkers (Pinteraction ≤ .004 and .001, respectively). Furthermore, among patients with OSCC, the C/T + T/T genotypes and T allele were associated with a decreased risk of advanced pathologic stage (P = .032) and lymph node involvement (P = .017).

Conclusions: BQ chewers carrying the T allele or C/T + T/T genotypes in pri-mir-26a-1 may have a decreased risk of oral leukoplakia, OPLs, and advanced-stage OSCC.

MeSH terms

  • Adult
  • Areca*
  • Carcinoma, Squamous Cell / chemically induced
  • Carcinoma, Squamous Cell / genetics*
  • Case-Control Studies
  • Disease Progression
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Male
  • MicroRNAs / genetics*
  • Middle Aged
  • Mouth Neoplasms / chemically induced
  • Mouth Neoplasms / genetics*
  • Phenotype
  • Polymorphism, Single Nucleotide*
  • Precancerous Conditions / chemically induced
  • Precancerous Conditions / genetics*
  • Risk Factors

Substances

  • MIRN26A microRNA, human
  • MicroRNAs