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Background: p53 acts as both a tumor-suppressor and transcription factor that, upon activation by DNA damage and other cellular stress signals, leads to the transcription of genes triggering cell-cycle arrest, apoptosis, and DNA repair (1,2). The gene for the nuclear phosphoprotein p53 is the most commonly mutated gene yet identified in human cancers (3). p53 is frequently mutated or inactivated in about 60% of cancers (4,5). Cyclin dependent kinase 9, whose well-known substrate is RNA polymerase II, can also phosphorylate p53, more specifically, Ser33 on the N-terminus and, Ser315 and Ser392 on the C-terminus (6).