Molecular epidemiology of DNA repair gene polymorphisms and head and neck cancer

Meilin Wang1, Haiyan Chu, Zhengdong Zhang

  • 1Department of Genetic Toxicology, the Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, China; ; Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu 211166, China;

Insights

Single nucleotide polymorphisms (SNPs) in DNA repair genes show limited association with head and neck cancer (HNC) risk. Further pathway-based analyses are needed to understand genetic susceptibility in HNC.

Area of Science:

  • Oncology
  • Genetics
  • Epidemiology

Background:

  • Head and neck cancer (HNC) is influenced by tobacco and alcohol, but genetic susceptibility and viral infections require further investigation.
  • Interindividual differences in HNC risk may stem from interactions between genetic variants and environmental exposures, particularly DNA damage.
  • Single nucleotide polymorphisms (SNPs) in DNA repair genes are implicated as risk factors in various cancers, including HNC.

Purpose of the Study:

  • To review epidemiological studies on the association between HNC risk and SNPs in DNA repair genes.
  • To examine the roles of various DNA repair pathways, including base-excision repair, nucleotide-excision repair, mismatch repair, double-strand break repair, and direct reversion repair.

Main Methods:

  • Systematic review of epidemiological studies investigating HNC risk and SNPs in DNA repair genes.
  • Analysis focused on specific DNA repair pathways and their associated genetic variants.

Main Results:

  • Few SNPs in DNA repair genes demonstrated a statistically significant association with increased or decreased HNC risk.
  • Observed associations were generally moderate and often dependent on locus-locus interactions among risk SNPs within repair pathways.
  • The overall contribution of individual SNPs in DNA repair genes to HNC risk appears limited.

Conclusions:

  • Current evidence suggests a modest role for individual SNPs in DNA repair genes regarding HNC risk.
  • Further genome-wide association studies (GWASs) incorporating pathway-based analyses are necessary to elucidate the genetic architecture of HNC susceptibility, especially in the context of environmental exposures.