Cancer is a cluster of diseases which involves variation in the status and activation of multiple genes that impart an advantage to survive and unexhausting proliferative potential to somatic or germinal cells (Cho 2007). The three main classes of genes altered primarily are proto-oncogenes, tumor suppressor genes, and DNA repair genes. Together they contribute to the growth of cancer phenotype and genotype to defend against the natural and inherent death mechanisms ingrained in cells as apoptosis and like processes, associated with deregulation of cell proliferation events. Apart from this, there is also an escalating evidence to recommend that cancer is also driven by epigenetic changes like DNA methylation and transformed patterns of histone modifcations resulting in variation in chromatin condensation status, hence regulating activation of certain set of specifc genes (Ediriwickrema and Saltzman 2015; Bayli and Ohm 2006). Most cancers are named according to their origin of sites in which they begin like cancer that originates in the renal proximal cells is called renal cell carcinoma and renal pelvis carcinoma is the cancer that originates in the center of the kidney where urine collects. Wilms tumor usually develops in children under the age of 5 (Bhatt et al. 2010).