ial chemosensitizing adviser. Interestingly, we realized that, though CDDP failed to activate ERK, its connection with DCPE triggered a strong stimulation of DCPEinduced activation of ERK. Perhaps the inhibition of the phosphatase often by DCPE or by CDDP is involved remains to be investigated. In summary, we’ve demonstrated that DCPE induced ERK activation, G0/G1 HDAC8 inhibitor arrest and apoptosis in cisplatinresistant OAW42 R cells. Furthermore, these results were correlated with p21WAF1/CIP1 induction, Bcl 2 inhibition and, to a lower extent, with Bcl xL inhibition in this cell line. DCPE applied also a cytotoxic and/or cytostatic effect on three other ovarian carcinoma cell lines. Sensitivity to the particle seemed to be in particular linked with the introduction of ERK phosphorylation in cells that didn’t present any basal activation of the path, as opposed to with a top degree of phospho ERK alone. Additionally, we confirmed that DCPE sensitized OAW42 R resistant cells to the cytotoxic effect of cisplatin, which increased the effect of DCPE on ERK activation. DCPE and CDDP could hence constitute reciprocal chemosensitizing agencies. Collectively, our results highlighted the possible interest of DCPE, used alone o-r along with cisplatin, for the treatment of ovarian Cellular differentiation carcinoma. In addition they suggested that the lack of basal G ERK may possibly constitute a predictive marker of response to this novel treatment. Ovarian carcinoma is the best cause of death among women with gynecologic malignancies. Following main medical cytoreduction, the initial line chemotherapy is essentially according to platinum compounds, in combination chemotherapy regimens. Even though that the majority of ovarian tumors are painful and sensitive to chemotherapy when individuals first present with the disease, pan Chk inhibitor recurrence and chemoresistance that is received during the course of treatments stay major obstacles to successful treatment. Connected with late diagnosis, this leads to a standard 5-year survival rate of approximately 2500-10 for patients with high level stage illness. Despite improvements in surgical practices and the introduction of taxanes in treatment protocols, this survival rate has not increased significantly over the past 25-years.. The development of new therapies for ovarian carcinoma may include two broad approaches. The very first one consists in improving the efficacy of active drugs with established activity in this disease, like cisplatin. The next one consists in modulating distinct molecular targets to induce apoptosis, without using conventional chemotherapy. Thus, proteins or pathways that are necessary for proliferation and carcinoma cell survival either in the absence or in the pres-ence of cisplatin can represent targets of inhibition. On the other side, apoptotic proteins or pathways, that are dropped in cancer cells or in response to the chemotherapeutic agent, could be restored.