Association of DNA repair genes polymorphisms and mutations with increased risk of head and neck cancer: a review.
Agata DylawerskaWojciech BarczakAnna WegnerWojciech GolusinskiWiktoria Maria SuchorskaPublished in: Medical oncology (Northwood, London, England) (2017)
DNA repair mechanisms allow maintain genomic stability and proper functioning within the cells. Any aberrations may cause an increased risk of many diseases such as cancer. The most crucial risk factors for head and neck squamous cell carcinoma are behavioral factors, predominantly chronic exposure to tobacco, alcohol addiction, and infection with human papillomavirus or Epstein-Barr virus. These agents can induce DNA damage; therefore, cells must activate appropriate mechanisms in order to function correctly. Cancer cells are marked with genomic instability, which is associated with a greater tendency for the accumulation of a DNA damage and increased chemo- and radioresistance. Multiple studies have assessed the correlation of increased head and neck cancer (HNC) risk with polymorphism in the DNA repair genes. However, they suggest that interaction of DNA repair genes mutations with susceptibility to HNC depends on a patient's race and risk factors, especially tobacco smoking. Further identification of these sequence variations must be performed. In this review, we discuss the current knowledge about the DNA repair genes mutations and polymorphisms associated with the high risk of head and neck treatment.
Keyphrases
- dna repair
- dna damage
- dna damage response
- bioinformatics analysis
- epstein barr virus
- genome wide
- induced apoptosis
- oxidative stress
- risk factors
- genome wide identification
- cell cycle arrest
- copy number
- healthcare
- squamous cell carcinoma
- dna methylation
- papillary thyroid
- cell death
- radiation therapy
- lymph node metastasis
- drug delivery
- squamous cell
- alcohol consumption
- signaling pathway
- young adults
- replacement therapy