Carcinogen metabolism, DNA damage repair and oral head and neck squamocellular carcinoma (HNSCC). A review.

Head and neck squamocellular carcinoma (HNSCC) has now become the 6th most common cancer among men in the developed world and affects the oral cavity, salivary glands, larynx and pharynx. Tobacco chewing, alcohol consumption and last but not least, smoking seem to be the most important risk factors. In particular in non-drinkers, smoke increases the relative risk (RR) of developing HNSCC of the oral cavity and pharynx from 2 to 20 fold; especially in the oral cavity, the association between alcohol and smoke could have a multiplier effect. Cancer arises from damage to DNA of genes located at various points of the short (p) and long (q) arms of a number of chromosomes, caused by exposure to various carcinogens. Thus, the carcinogenic process requires continuous exposure to environmental carcinogens (i.e., longstanding history of smoking and drinking), an increased susceptibility to carcinogens (induced by xenobiotic metabolizing enzyme polymorphism) and an impaired DNA repair capacity (both inherited and acquired). Our purpose in this paper is to review advances in the understanding of the role of the European or Caucasian genetic aberrations that affect carcinogen metabolism and DNA repair genes in oral HNSCC development: we consider that those abnormalities will be useful in assessing individuals at risk.