SUSCEPTIBILITY TO ORAL SQUAMOUS CELL CARCINOMA: CORRELATION WITH VARIANTS OF CYP1A1-MspI, GSTT1, GSTM1, ALDH2, EC-SOD AND LIFESTYLE FACTORS
Dong T-T, Wang L-J, Liu L-Z, Ma S-N
*Corresponding Author: Mrs. Ting-Ting Dong, General Hospital of Daqing Oil Field, No. 9 Zhongkang Street, Saertu District, Daqing 163001, Heilongjiang Province, People’s Republic of China. Tel: +86-459-599-4114. Fax: +86-459-580-5247. Email: tingtingdong_139@163.com
page: 61

INTRODUCTION

Head and neck squamous cell carcinoma (HNSCC) is a common malignancy that ranks sixth in incidence of all cancers. The HNSCC tumors display dysregulation of cell differentiation, cell cycle control, epithelial and stromal interactions, apoptosis, angiogenesis and their associated pathways [1,2]. Although its exact cause remains unclear, like most malignancies, HNSCC pathogenesis is affected by both genetic and environmental factors [1]. Of the approximately 500,000 new cases of HNSCC each year, many occur in the oral cavity, pharynx, and larynx. Oral squamous cell carcinoma (OSCC) is the most common type of HNSCC, and China has one of the highest incidences of this cancer [2]. Importantly, OSCC is nearly asymptomatic, which makes early diagnosis very difficult; to date, there are no accurate predictors of OSCC onset and/or progression. Therefore, identification of risk factors and high-risk populations for OSCC would enable advancements in the primary and secondary prevention of OSCC. Cigarette smoking and alcohol consumption are known environmental risk factors for OSCC [3,4]. Cigarette smoke contains polycyclic aromatic hydrocarbons, heterocyclic amines, and nitrosamines that are all carcinogenic. Long-term alcohol consumption can lead to combined overdose of reactive oxygen species (ROS) and acetaldehyde, inducing carcinogenesis. Certain enzymes have been shown to be responsible for the biotransformation of chemical carcinogens, either for activation or excretion. For example, cytochrome P4501A1, encoded by CYP1A1, is a catabolite-activating enzyme involved in the biotransformation of both tobacco and alcohol. P4501A1- mediated metabolism of tobacco combustion products, mainly polycyclic aromatic hydrocarbons, can lead to the formation of DNA adducts that contribute to tumor formation, specifically HNSCC [5]. Other metabolizing enzymes, with variations in their respective genes, have also been previously implicated in cancer susceptibility. These include, but are not limited to, glutathione S-transferase (GST), superoxide dismutate (SOD), proteins of the SOD family, and acetaldehyde dehydrogenase (ALDH). Glutathione S-transferase plays a role in metabolizing benzo[a]pyrene (a tobacco-specific carcinogen), as well as other carcinogenic compounds. Superoxide dismutase, an endogenous antioxidant enzyme, has certain polymorphisms implicated in cancer susceptibility. Acetaldehyde dehydrogenase, along with alcohol dehydrogenase (ADH), metabolizes ethanol by breaking apart the molecule in order to eliminate it from the body. Genetic polymorphism in ALDH2 has been previously investigated and shown to be associated with specific cancer types [5]. However, genes encoding these enzymes have multiple functional variants, blurring their role in OSCC susceptibility. At least one recent study found that expression of CYP1A1 and ALDH2 proteins did not affect OSCC prognosis [6]. Thus, the specific contribution of polymorphisms in genes encoding enzymes involved in biotransformation of alcohol and tobacco components remains unclear; specifically, the role in promoting OSCC requires further study. This study reports the investigation of the association between genetic polymorphism of CYP1A1, EC-SOD (extracellular SOD), GSTT1, GSTM1, ALDH2, smoking and alcohol consumption, and susceptibility to oral squamous cell carcinoma.



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