This study focused on the AF9 gene at 9p22, a common deletion region in NPC. Upon erroneous DNA repair, cells that survive apoptosis may harbor chromosomal rearrangements contributing to NPC pathogenesis. We hypothesized that oxidative stress-induced apoptosis may cause chromosomal breaks mediated by CAD. Eventually, the surviving cells may carry rearranged chromosomes. Although apoptosis is a cell death process, cells possess the potential to survive apoptosis upon DNA repair. Most of the NPC etiological factors are known to induce oxidative stress. Oxidative stress, which has been strongly implicated in carcinogenesis, is a potent apoptotic inducer. There are increasing evidences that the apoptotic nuclease caspase-activated deoxyribonuclease (CAD) is one of the players leading to translocation in leukemia.
Genetic aberrations have been identified in nasopharyngeal carcinoma (NPC), however, the underlying mechanism remains elusive.
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