It is in terms of a cell cycle that potentially renders the dividing cell exquisitely sensitive to dynamics of an apoptosis program that the preset dimensions of acquisition of stem cell attributes further conform to dimensions of a potential malignant transformation step. The hallmark of carcinogenesis as genomic instability arises within a cyclic setting of whole susceptible and dividing cells that project as derived gene amplification and over-expression. Aurora kinases are central determinants in the contrast profiling of apoptosis and of cell cycling in specific dimensions of genomic instability. The further derived models of a malignant transformation are inductive and further realized in terms of the cell that inherently cycles and determines whole arrayed sets of susceptibility issues in evolving transformation.