Grb2 is not the main signaling issue involved in ERK activated cell division, it’s reasonable that peptidimer c exhibits lower exercise on Bcr Abl over expressing cells in comparison with those over expressing HER2. The consequence of peptidimer d was also tried on the cell cycle. To the best of our understanding, only few reports have described the consequence of Grb2 inhibitors on cell cycle. In 2005, ROCK inhibitors Kim et al. described the result of actinomycin, an of Grb2 SH2 domain on cell cycle. In this study, they have shown, by proteomic analysis, that this compound is able to up regulate MEKK3 and to down regulate Hsp70 expression, which was correlated with G1 arrest of cell cycle. Within our case, peptidimerc, which will be an of Grb2 SH3 areas, induces S stage arrest, concomitantly with down regulation of cyclin A. In 2001, Shen natural compound library and Guan showed that targeting of Grb2 to focal contacts increased cell cycle progression, and biochemical studies related ERK activation in the form of Grb2, with its stimulation of cell cycle progression. Urogenital pelvic malignancy This observation supported the important part of Grb2 in cell cycle progression. The cell cycle is the process where cells replicate themselves, grow, and prepare to divide. Many respected reports revealed that ERK activation is associated with either activation or inhibition of cell proliferation. Activation of ERK process induced by growth facets and cytokines come into over expression of cyclin D and cyclin E which are G1 related cyclins. In many cases, blocking this indication arrested the cells in G1 phase, but various other data reported that ERK pathway initial also managed the progression of G2/M phase. In our studies, Gleevec triggered G1 arrest of K562 cells after treatment for 24 h, while peptidimer c charged cell cycle progression in S phase. Cabozantinib FLt inhibitor This result clearly demonstrated that the 2 drugs affect the cell cycle of K562 cells by different mechanisms. Pytel et al. also showed that the therapy with Gleevec reduced fraction of K562 cells in G2/M gate and retrieved normal cell cycle process. Moreover, the inhibition of Bcr Abl tyrosine kinase by Gleevec caused both cell cycle arrest in the G0/G1 phase and increased the part of apoptotic cells, and the reduction of cyclin D2 may possibly contribute to the G0/G1phase arrest. Cell cycle progression involves the activation and interaction of cyclins and cyclindependent kinases. Cyclin A is required for the initiation of cell DNA synthesis in the S phase and the entry in G2/M phase, while cyclin D is the main element regulator for G0/ G1 to S phase progression, and cyclin B is related to G2/M phase.