Have been searching the internet as I do every night. I'm on Doxil and Avastin after second recurrence and finding out I'm platinum resistant. I googled the following: Chemo with longest survival rate for OVCA.
This is what popped upL Effect of mifepristone used alone or with cisplatin chemotherapy on human ovary cancer cell growth
by Freeburg, Elizabeth McKay, Ph.D., University of South Dakota, 2008, 163 pages; AAT 3351178
Ovarian cancer (OvCa) causes more deaths than any other gynecologic malignancy. It is usually diagnosed at late stages and patients require cytoreductive surgery followed by platinum-based chemotherapy. However, the efficacy of platinum derivatives is hindered by their elevated toxicity, the development of tumor tolerance to the drugs, and the regrowth or repopulation of tumor cells between treatment intervals. Hence, search for new measures to enhance the efficacy of platinum derivatives for OvCa is imperative. Preclinical studies in our laboratory have demonstrated that the antiprogestin steroid, mifepristone (MF), is effective as a single agent in vitro and in vivo inhibiting growth of human epithelial OvCa cells. MF induces a reversible blockage of the cell cycle at the G1-to-S transition and a strong inhibition of cyclin dependent kinase 2 (Cdk2) activity. Based on these data and the fact that Cdk2 is frequently up-regulated in ovarian tumors, this project was developed to test the hypothesis that MF enhances the efficacy of platinum-based therapy--utilizing cisplatin (CDDP) as a prototype. First, we sought to determine if the cytostatic concentrations of MF prevents repopulation of OvCa cells occurring between CDDP treatment intervals. Evidence is presented on the generation of an in vitro model of OvCa repopulation between CDDP rounds, its efficient abrogation by MF, and the apparent enhancement of CDDP-induced toxicity by MF. Secondly, we asked whether the toxicity of MF occurred regardless of the degree of sensitivity developed by the OvCa cells to CDDP, and of the status of the p53 tumor suppressor gene. Evidence is presented suggesting that MF-induced cytotoxicity involving cytostasis at low concentrations, and caspase-associated apoptotic lethality at high concentrations, does not correlate with the sensitivity of the cells to CDDP, and appears to be independent of the p53 genetic status. Overall, our studies provide evidence to suggest that MF used either alone or together with CDDP has the potential to improve OvCa treatment success. Using MF therapy in association with, and after platinum chemotherapy, may significantly improve the 5 year survival rate for OvCa, and conceivably convert this lethal cancer into a treatable chronic disease.
So I'm wondering anyone ever on this trial? Any other info?