NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. Temozolomide (TMZ), an alkylating agent, is widely used for treating primary and recurrent high-grade gliomas. Metabolism of chloroquine Plaquenil side effects antimalarial Chloroquine resistance mechanism Activation of the p53 growth suppression/apoptotic pathway is one of the promising strategies in targeting glioma cells. We show that the quinoline derivative chloroquine activates the p53 pathway and suppresses growth of glioma cells in vitro and in vivo in an orthotopic U87MG human glioblastoma mouse model. All above, these data support that NTZ exhibits anti-glioma properties in vivo. Fig. 6 NTZ inhibits glioma growth in vivo. a Dissected tumors from a xenograft model with or without 27-day NTZ. For instance, some of in vitro research data laid a foundation to initiate clinical trials such as data showing that chloroquine treatment might create benefits for glioma patients, since it may sensitize glioma cells to ionizing radiation via decreasing viable hypoxic fraction of tumor cells and autophagy. Recently, studies have found that TMZ treatment could induce autophagy, which contributes to therapy resistance in glioma. However, the efficacy of TMZ is often limited by the development of resistance. Glioma chloroquine in vivo Chloroquine activates the p53 pathway and induces apoptosis., Nitazoxanide, an antiprotozoal drug, inhibits late-stage. Chloroquine injection routeHydroxychloroquine and mood swings In vitro, U373 cells engineered to overexpress EGFR were more sensitive to chloroquine treatment than unaltered U373 glioblastoma cells. Other publications by this group showed an increased dependence of EGFR overexpressing cancer cells on autophagy, while chloroquine is a known autophagy inhibitor. Repurposed Drugs Astrocytoma Options. Autophagy in glioma cells An identity crisis with a clinical.. The COC Protocol in Glioma - Care Oncology US. However, GBM typically has large areas of hypoxia in the center of the tumor, and autophagy is a natural coping mechanism to this natural hypoxia. Also bevacizumab tends to increase hypoxia, and is likely the reason BEV + chloroquine was shown to be synergistic in mouse models. Mar 14, 2016 Glioblastoma multiforme GBM is the most aggressive and common brain tumor in adults. Sorafenib, a multi-kinase inhibitor, has been shown to inhibit cell proliferation and induce apoptosis through inhibition of STAT3 signaling in glioblastoma cells and in intracranial gliomas. Temozolomide TMZ, an alkylating agent, is widely used for treating primary and recurrent high-grade gliomas. However, the efficacy of TMZ is often limited by the development of resistance. TMZ treatment could induce autophagy, which contributes to therapy resistance in glioma.