The mode of action by radiation is postulated to be the production of double strand breaks of DNA. The repair of double strand breaks occurs through non homologous end joining through acetylation of histone proteins by histone acetyltransferases (HATs). The fixation of double strand breaks through HAT inhibitors is a promising application for radiation sensitization in the clinic.
P53 is a tumour suppressor gene and its mutation has been implicated in 60% of human cancers. As one of the pivotal anticancer genes, P53 controls the transcription and translation of a series of genes. The kinetics of DNA double strand break generation and their co relation to P53 status, ATM and ARF activation are computed and modelled for understanding the potential of such research.