Fig. 7

A potential model for oxidative stress-induced chromosomal rearrangement in NPC. NPC etiological factors, such as EBV infection, nitrosamine, cigarette smoke, wood dust and formaldehyde may trigger oxidative stress. PS externalization and disruption of MMP, which are recognized as apoptotic signaling, initiate oxidative stress-induced apoptosis. This in turn leads to caspase-3 activation. Upon cleavage of ICAD by caspase-3, CAD is released from its chaperone, ICAD, to cleave chromosomal DNA within BCR. The cells try to evade from apoptosis through imprecise DNA repair. Cells that survive apoptosis may carry chromosomal rearrangements such as deletion and amplification which contribute to tumorigenesis of NPC