الفهرس 
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Abstract
Cancer is a disease caused by corruption of normal biological circuits and processes leading to uncontrolled proliferative growth, it is always characterized by a complex range of alterations that affect multiple scales ranging from molecular activity within cells to communication between cells and tissues (Du and Elemento 2014). At the genomic level, cancer cells are characterized by frequent disruption of the DNA maintenance machinery and epigenetic modifiers result in thousands of sequence alterations and global epigenetic reprogramming (Vogelstein et al. 2013).The rate of mutation and chromosomal abnormalities in normal cells is kept low by reliable DNA damage response pathways, while, in cancer cells, oncogene-induced DNA replication stress and/or direct disruptions of DNA repair genes frequently occur, results in widespread genomic instability (Negrini et al. 2010). A good example for that is, p53, an essential protein for DNA damage response that is frequently mutated in cancer across many tumor types (Muller and Vousden 2013).