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    Home > Active Ingredient News > Antitumor Therapy > Ways to enhance the effectiveness of dasateni in treating diffuse endogenesian bridge gliomas.

    Ways to enhance the effectiveness of dasateni in treating diffuse endogenesian bridge gliomas.

    • Last Update: 2020-10-15
    • Source: Internet
    • Author: User
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    Diffuse endogenetic bridge glioma (diffuse intrinsic pontine glioma, DIPG) is a malignant brain tumor that cannot be surgically removed, accounting for about 10% of the central nervous system tumors in children.
    total survival (OS) of DIPG is only 9 months, and there is currently no effective treatment.
    the drug excrete effects of blood-brain barrier (BBB) permeability and ATP binding cassette (ABC) transporter (e.g. P-glycoprotein) may be the reason for the poor efficacy of drug treatment DIPG.
    enhanced drug convection(convection-enhanced delivery, CED) is a way to increase BBB permeability.
    addition, knocking out or inhibiting ABC transporters can increase the concentration of drugs inside tumors and promote tumor apoptosis.
    plateboard-derived growth factor acceptor (PDGFR) is a widely expressed cancer gene in DIPG and can be used as a therapeutic target.
    dasatinib targets PDGFR, but can be transported by ABC.
    Vadim Tsvankin of Neurosurgery at Duke University Medical Center in Carolina, USA, and others studied the efficacy of ABC transporter inhibitors tariquidar and CED infusion dasatinib in the treatment of DIPG, the results of which were published in the May 2020 issue of Neurosurgery.
    results, the results showed that the overall lifetime of DIPG animal models (OS) was significantly extended by the CED's continuous infusion of dasatinib compared with the control group: 39.5d:28.5d (P=0.0139).
    of 274 children with brain and systemic solid tumors, ABCB1 had the highest expression among high-level gliomas (HGG) with H3.K27M mutations (Figure 1), higher than in other children with non-gliomas (P<0.05).
    1. Of the 274 children with solid brain and systemic tumors, ABCB1 had the highest level of expression in the high-level glioma (HGG) of the K27M mutation.
    in-body tumor cells found that dasatinib significantly reduced tumor cell activity (P<05) compared to the control group.
    the efficacy of tariquidar and tessamisong to further improve the efficacy of dasatinib (P<0.001).
    in vivo animal models found that the bits of CED infusions of dasatinib showed low signals on MRI-T1 weighted imaging, surrounded by high signals and uneven signals (Figure 2).
    addition, tariquidar and dexamisson pre-treatment did not affect the distribution of CED infusions in the body.
    2. The pre-treatment of dexamisson and tariquidar does not affect the distribution of CED infusion dasatinib in the body.
    immunoglostification study found that the number of CC3-positive cells in the combined Dasatinib treatment group of dexamisson and tariquidar pretreated was higher than in the single-use dasatinib group and control group (P<0.001); Under the mirror, 1050±410/field of view are visible, compared with 785±160/field of view in the single-use dasatinib group and 334.2±109/field of view in the control group (Figure 3).
    , there was no significant difference in the number of Ki67-positive cells in each group.
    Figure 3. DIPG mice were dyed with summytin, CC3 and Ki67 immunogroups.
    number of CC3-positive cells in the combined Dasatinib treatment group with terrestress and tariquidar pretreated was significantly higher than in the single-use dasatinib treatment group or control group.
    also found that the mid-OS in the single-use dasatinib treatment group of DIPG animal models was 39d, compared with 31.5d in the control group, and 49d in the DIPG animal models in the Tariquidar and Desamisson pretreated groups, significantly longer than the previous two groups (P=0.0092) (Figure 4).
    Figure 4. DIPG mouse model Kaplan-Meier survival curve.
    the survival of the combined dasatinib treatment group of the terrestress and tariquidar pretreatments was significantly extended (P=0.0092).
    Conclusions The results of this study show that the ABC transporter inhibitor (tariquidar) combined with the samisson application can improve the effect of CED infusion dasatinib in treating THEPG animal models of H3.3K27M mutations, such as promoting tumor cell death and prolonging survival.
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