The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Yunzhi Yang - One of the best experts on this subject based on the ideXlab platform.
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a chitosan β glycerophosphate thermo sensitive gel for the delivery of ellagic acid for the treatment of Brain Cancer
Biomaterials, 2010Co-Authors: Sungwoo Kim, Satoru K Nishimoto, Joel D Bumgardner, Warren O Haggard, Waleed M Gaber, Yunzhi YangAbstract:We report here the development of a chitosan/beta-glycerophosphate(Ch/beta-GP) thermo-sensitive gel to deliver ellagic acid (EA) for Cancer treatment. The properties of the Ch/beta-GP gels were characterized regarding chemical structure, surface morphology, and viscoelasticity. In vitro EA release rate from the EA loaded Ch/beta-GP gel and chitosan degradation rate were investigated. The anti-tumor effect of the EA loaded Ch/beta-GP gel on Brain Cancer cells (human U87 glioblastomas and rat C6 glioma cells) was evaluated by examining cell viability. Cell number and activity were monitored by the MTS assay. The Ch/beta-GP solution formed a heat-induced gel at body temperature, and the gelation temperature and time were affected by the final pH of the Ch/beta-GP solution. The lysozyme increased the EA release rate by 2.5 times higher than that in the absence of lysozyme. Dialyzed chitosan solution with final pH 6.3 greatly reduced the beta-GP needed for gelation, thereby significantly improving the biocompatibility of gel (p < 0.001). The chitosan gels containing 1% (w/v) of ellagic acid significantly reduced viability of U87 cells and C6 cells compared with the chitosan gels at 3 days incubation (p < 0.01, and p < 0.001, respectively).
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a chitosan β glycerophosphate thermo sensitive gel for the delivery of ellagic acid for the treatment of Brain Cancer
Biomaterials, 2010Co-Authors: Satoru K Nishimoto, Joel D Bumgardner, Warren O Haggard, Waleed M Gaber, Yunzhi YangAbstract:We report here the development of a chitosan/β-glycerophosphate(Ch/β-GP) thermo-sensitive gel to deliver ellagic acid (EA) for Cancer treatment. The properties of the Ch/β-GP gels were characterized regarding chemical structure, surface morphology, and viscoelasticity. In vitro EA release rate from the EA loaded Ch/β-GP gel and chitosan degradation rate were investigated. The anti-tumor effect of the EA loaded Ch/β-GP gel on Brain Cancer cells (human U87 glioblastomas and rat C6 glioma cells) was evaluated by examining cell viability. Cell number and activity were monitored by the MTS assay. The Ch/β-GP solution formed a heat-induced gel at body temperature, and the gelation temperature and time were affected by the final pH of the Ch/β-GP solution. The lysozyme increased the EA release rate by 2.5 times higher than that in the absence of lysozyme. Dialyzed chitosan solution with final pH 6.3 greatly reduced the β-GP needed for gelation, thereby significantly improving the biocompatibility of gel (p < 0.001). The chitosan gels containing 1% (w/v) of ellagic acid significantly reduced viability of U87 cells and C6 cells compared with the chitosan gels at 3 days incubation (p < 0.01, and p < 0.001, respectively).
Antonella Pignata - One of the best experts on this subject based on the ideXlab platform.
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retraction note a homing system targets therapeutic t cells to Brain Cancer
Nature, 2019Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
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a homing system targets therapeutic t cells to Brain Cancer
Nature, 2018Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
Julien Dubrulle - One of the best experts on this subject based on the ideXlab platform.
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retraction note a homing system targets therapeutic t cells to Brain Cancer
Nature, 2019Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
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a homing system targets therapeutic t cells to Brain Cancer
Nature, 2018Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
Fong W Lam - One of the best experts on this subject based on the ideXlab platform.
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retraction note a homing system targets therapeutic t cells to Brain Cancer
Nature, 2019Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
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a homing system targets therapeutic t cells to Brain Cancer
Nature, 2018Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
Heba Samaha - One of the best experts on this subject based on the ideXlab platform.
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retraction note a homing system targets therapeutic t cells to Brain Cancer
Nature, 2019Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.
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a homing system targets therapeutic t cells to Brain Cancer
Nature, 2018Co-Authors: Heba Samaha, Antonella Pignata, Kristen Fousek, Jun Ren, Fong W Lam, Fabio Stossi, Julien DubrulleAbstract:Successful T cell immunotherapy for Brain Cancer requires that the T cells can access tumour tissues, but this has been difficult to achieve. Here we show that, in contrast to inflammatory Brain diseases such as multiple sclerosis, where endothelial cells upregulate ICAM1 and VCAM1 to guide the extravasation of pro-inflammatory cells, Cancer endothelium downregulates these molecules to evade immune recognition. By contrast, we found that Cancer endothelium upregulates activated leukocyte cell adhesion molecule (ALCAM), which allowed us to overcome this immune-evasion mechanism by creating an ALCAM-restricted homing system (HS). We re-engineered the natural ligand of ALCAM, CD6, in a manner that triggers initial anchorage of T cells to ALCAM and conditionally mediates a secondary wave of adhesion by sensitizing T cells to low-level ICAM1 on the Cancer endothelium, thereby creating the adhesion forces necessary to capture T cells from the bloodstream. Cytotoxic HS T cells robustly infiltrated Brain Cancers after intravenous injection and exhibited potent antitumour activity. We have therefore developed a molecule that targets the delivery of T cells to Brain Cancer.