“…Several factors come into play in the regulation of cdk2 activity, such as binding of cdk2 inhibitors as p21 waf1 , p27 Kip1 , and p57 Kip2 (Malumbers and Barbacid, 2005), the already mentioned transient associations with cyclins A and E (Giordano et al, 1989(Giordano et al, , 1991Koff et al, 1992;Bates et al, 1994) and phosphorylation of specific tyrosine and threonine residues (Gu et al, 1992). The constitutive activation of cdk2/cyclin E complexes is often associated with the deregulation of G1 to S transition and tumor progression (Fujii et al, 1998;Harwell et al, 2004;Ioachim et al, 2004;Liao et al, 2004;Sunters et al, 2004;Peschos et al, 2005;Tenderenda, 2005). On these grounds, the targeting of cdk2 activity can have important implications for the development of therapeutics for cancer treatment.…”