在亞洲，口腔癌是常見的一種惡性腫瘤，在台灣更是男性癌症死亡率的第五位。咀嚼含菸葉的檳榔塊是造成口腔癌發生的主要原因，同時也與口腔下纖維化的發生有關。有許多研究證實咀嚼檳榔塊在口腔會產生活性氧化物。因為暴露在有毒物質下或因保護因子不夠，而導致過多活性氧化物的產生，可能會對細胞膜核甘酸及蛋白質等產生氧化性傷害。檳榔塊中的纖維在咀嚼的過程中，在口腔內膜造成的物理性創傷，可能會促使白血球細胞的侵潤，此時骨髓過氧化酵素會被釋放出，並產生活性氧化物。骨髓過氧化酵素基因在-463GA的取代，會造成轉錄的表現降低，因而酵素的表現及活性氧化物的產生也因而降低。因此本計劃的目的就是要來探討這三種酵素的基因多型性與口腔癌及口腔下纖維化之危險因子間的關係性。 Oral squamous cell carcinoma (OSCC) is one of the most common malignant neoplasms in Asia countries, and is the fifth cause of male cancer mortality in Taiwan. Chewing betel quid (BQ) containing tobacco was found to contribute to the development of OSCC, and be causally linked to oral submucous fibrosis (OSF), a potentially malignant condition of the oral cavity. Previous studies found that chewing BQ generates reactive oxygen species (ROS) in oral cavity. The excessive formation of ROS may result from exposure to toxic agents and/or insufficiency of defense mechanisms, which might cause oxidative damage to the cellular membranes, DNA, and proteins. The fiber of BQ may cause physically injury of oral mucus membrane and neutrophils will be recruited and accumulate at the sites around oral mucosal lesions. Subsequently, myeloperoxidase (MPO) is released into the local environment and generate ROS. The -463GA substitution in the promoter region of the MPO gene has been associated with a decrease in transcriptional expression and thus reduced enzyme levels were available for the formation of ROS. Therefore, the objective of our study is to investigate the association of MPO with BQ-related OSCC/OSF.
