Into an important goal. This k More light nnte to the use of mTOR inhibitors in future clinical trials. Rapamycin analogs Although limited, there are KU-0063794 reports of in vitro and pr Clinical studies, the efficacy of rapamycin analogues CCI-779 and RAD 001 in the treatment of prostate cancer. CCI 779 inhibited the growth of PC3 and DU 145 cells in a dose-dependent Ngigen manner reduces in vitro and in vivo tumor volumes in the PC 3 and DU-145 xenografts. RAD 001 entered treatment Born in reduced proliferation of cancer cells in vitro and in vivo by a PIN-L Emissions HIF-dependent Independent paths in Act 1 transgenic M Mice reversed. There are no comparable published shall report on the Rapamycin AP23573 for prostate cancer today. Nevertheless, all three analogs, and rapamycin, is currently studying in clinical trials for the treatment of prostate cancer.
In experiments, a more efficient, much emphasis is available on the search for therapies for advanced prostate cancer with synergistic or additive effects Danoprevir Proteasome inhibitor have been. A challenge in the use of mTOR inhibitors, and other signal transduction is the overlapping of signal paths, erm Glicht the cells to bypass the target molecule when exposed to these inhibitors. Resistance to report transduction inhibitors probably caused by mutations in one of the most important factors in such a way that go to the signaling cascade or by up-regulation of alternative ways to survive the growth of the cell and allow various mechanisms can k. Therefore, many studies on the inhibition of mTOR in combination therapy focuses liked t as monotherapy.
A combination of rapamycin and inhibitors of tyrosine kinase receptor and a lower survival rate CWR22Rv1 LNCaP cells in vitro, and a combination of rapamycin and Dglucosamine obtained Hte growth inhibition DU 145 cells. Rapamycin in combination with a oligodeoxinucleotide insulin receptor Dovitinib substrate exposed antisense inhibition st Amplifier tumor growth of PC 3 of the treatment with the antisense an IRS. Inhibition of PC 3 and 2 C4 tumors was deactylase with the combination of rapamycin and histone either agent alone increased Ht. CCI 779 reversed resistance to doxorubicin-PC 3 and DU 145 tumors and have additive effects when used in combination with docetaxel. RAD 001 in combination with an inhibitor of epidermal growth factor receptor and a new antiandrogen VN/124 1 inhibitors have used additive effects on the growth of LNCaP cells in vitro.
RAD 001 sensitizes prostate cancer cells and radiation. We have recently shown that RAD 001 in combination with Zoledrons Acid and docetaxel effectively inhibited the growth of prostate tumor cells in the bone of the environment on any of these agents alone. INTERACTION between rail and PI3K/Akt/mTOR Androgen receptors, detailed studies have shown that the cross talk between the AR and PI3K/Akt/mTOR signaling pathways. AR is an important modulator of growth and development of the prostate and progression of prostate cancer. AR-mediated transcription is tightly controlled Lee and the mechanisms regulating the AR transcriptional activity t factor in cooperation with transcriptional cofactors, as well as phosphorylation and acetylation. A better fully understand the molecular interactions is an