rapamycin therapy considerably reduces the aftereffect of IGF 1 on Akt phosphorylation, indicating that drug can impair Akt activity by inhibiting mTOR in OPC cultures. We have now shown that rapamycin inhibited the effect of Hu-210 with this kinase. Finally, mTOR can be phosphorylated via Cilengitide PI3k/AKT signalling, and LY294002 inhibited Hu-210 induced phosphorylation of mTOR. These findings show the crosstalk between mTOR and PI3K/Akt during the procedure for cannabinoid activated oligodendrocyte differentiation. Together, the data presented here suggest that an up regulation in tone might be responsible for oligodendrocyte differentiation and provide evidence ofconcept that CB receptors and possible therapeutic targets 2 AG/DAGL act to counteract the increased loss of oligodendroglial cells. Consequently, intense activation of the neighborhood endocannabinoid system would have a profound positive impact on oligodendrocyte fate and subsequently, on brain repair. Consequently, we propose that the mind endocannabinoid system might well regulate the progression of demyelinating disorders such as multiple nucleophilic substitution sclerosis. Survival of chronic lymphocytic leukemia cells in vivo is supported by the tissue microenvironment, which includes aspects of the extracellular matrix. Interactions between cancer cells and the extra-cellular matrix are in part mediated by CD44, whose principle ligand in this respect is hyaluronic acid. Purpose: to evaluate the effect of CD44 involvement on the survival of CLL cells. Experimental Design: CD44 in CLL cells was employed by anti CD44 monoclonal antibody, or hyaluronic acid, and the consequences of CD44 activation on Dasatinib BMS-354825 prosurvival pathways and CLL cell viability were considered. Results: proposal of CD44 activated the MAPK/ERK and PI3K/AKT paths and increased MCL 1 protein expression. Consistent with the induction of these anti-apoptotic things, CD44 protected CLL cells from natural and fludarabineinduced apoptosis. Leukemic cells of the more aggressive CLL subtype that express unmutated IgVH genes showed higher CD44 expression than IgVH mutated CLL cells, and acquired a better survival advantage via CD44 initial. Ergo, CD44 activation in the tissue microenvironment might contribute to increased MCL 1 protein ranges, resistance to apoptosis, and might contribute to the more progressive character of U CLL. Moreover, PI3K or MEK inhibitors along with obatoclax, a villain of MCL 1, blocked the pro survival effect of CD44. Furthermore, obatoclax synergized with fludarabine to induce apoptosis of CLL cells. Conclusions: the different parts of the extracellular matrix may give survival signals to CLL cells through engagement of CD44. Inhibition of MCL 1, PI3K, and MAPK/ERK pathways are promising ways of decrease the anti apoptotic effect of the microenvironment on CLL cells.