Role of nonhomologous end-joining in oral cancer and personalized pharmacogenomics

Recent years have witnessed the incidence of cancer rise worldwide, with no end to the war against it in sight. It is believed that cancer emanates from a series of genetic alterations leading to the progressive disorder of the normal mechanisms that control cell proliferation, differentiation, death, and/or genomic stability. With our genome under constant exogenous and endogenous assault, cellular capacity to maintain genomic stability by means of various DNA repair mechanisms looms vital to preventing tumor initiation and progression. In the same vein, the relative role of DNA repair as biomarker for prognosis, predicator of drug and therapy response, or indeed as target for novel gene therapy, has been recently patented and is very promising. This paper summarizes studies probing association among nonhomologous end-joining genes XRCC4, XRCC5, and XRCC6 vis-à-vis oral cancer susceptibility, then discusses their role in carcinogenesis and personalized pharmacogenomics.