The Experts below are selected from a list of 235071 Experts worldwide ranked by ideXlab platform
Yunhui Liu - One of the best experts on this subject based on the ideXlab platform.
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knockdown of usf1 inhibits the vasculogenic mimicry of Glioma cells via stimulating snhg16 mir 212 3p and linc00667 mir 429 axis
Molecular therapy. Nucleic acids, 2019Co-Authors: Di Wang, Jian Zheng, Xiaobai Liu, Yixue Xue, Libo Liu, Heng Cai, Yunhui LiuAbstract:The anti-angiogenic treatment of malignant Glioma cells is an effective method to treat high-grade Gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of Gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in Gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in Glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in Glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of Glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of Glioma cells, and these findings might provide a novel strategy for Glioma treatment.
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Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis.
Molecular therapy. Nucleic acids, 2019Co-Authors: Di Wang, Jian Zheng, Xiaobai Liu, Yixue Xue, Libo Liu, Heng Cai, Yunhui LiuAbstract:The anti-angiogenic treatment of malignant Glioma cells is an effective method to treat high-grade Gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of Gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in Gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in Glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in Glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of Glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of Glioma cells, and these findings might provide a novel strategy for Glioma treatment.
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Study of correlation between expression of bradykinin B2 receptor and pathological grade in human Gliomas
British journal of neurosurgery, 2005Co-Authors: Yi-song Zhao, Yixue Xue, Yunhui Liu, Nai-jia Jiang, Ping Wang, Zhi-hang Yang, Yuqin WangAbstract:In clinical practice there is a difference in response of the blood-tumour barrier (BTB) permeability induced by bradykinin in brain tumours with the same pathology. The variability in response of tumours to bradykinin is likely to be related to the expression level of bradykinin B2 receptor. This study used fresh human Glioma samples to determine the expression level of bradykinin B2 receptor on Gliomas with different pathological grades. The grade of tumour was classified using the WHO classification. To determine the bradykinin B2 receptor expression level in Gliomas, Immunohistochemistry and Western blot methods were used. In 24 cases of Gliomas there were eight cases of WHO I Glioma, eight cases of WHO II Glioma and eight cases of WHO III Glioma. Both Western blot and immunohistochemistry showed bradykinin B2 receptors localized on tumour cells, whilst brain cells at the edge of the Glioma hardly expressed B2 receptor. There were significant differences of bradykinin B2 receptor expression level amon...
Aristotelis Tsirigos - One of the best experts on this subject based on the ideXlab platform.
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cell surface notch ligand dll3 is a therapeutic target in isocitrate dehydrogenase mutant Glioma
Clinical Cancer Research, 2019Co-Authors: Marissa Spino, Sylvia C. Kurz, Luis Chiriboga, Jonathan Serrano, Briana Zeck, Namita Sen, Seema Patel, Guomiao Shen, Varshini Vasudevaraja, Aristotelis TsirigosAbstract:Purpose: Isocitrate dehydrogenase (IDH) mutant Gliomas are a distinct Glioma molecular subtype for which no effective molecularly-directed therapy exists. Low-grade Gliomas, which are 80-90% IDH mutant, have high RNA levels of the cell surface Notch ligand DLL3. We sought to determine DLL3 expression by immunohistochemistry in Glioma molecular subtypes and the potential efficacy of an anti-DLL3 antibody drug conjugate (ADC), rovalpituzumab tesirine (Rova-T), in IDH mutant Glioma. Experimental Design: We evaluated DLL3 expression by RNA using TCGA data and by immunohistochemistry in a discovery set of 63 Gliomas and 20 non-tumor brain tissues and a validation set of 62 known IDH wildtype and mutant Gliomas using a monoclonal anti-DLL3 antibody. Genotype was determined using a DNA methylation array classifier or by sequencing. The effect of Rova-T on patient-derived endogenous IDH mutant Glioma tumorspheres was determined by cell viability assay. Results: Compared to IDH wildtype glioblastoma, IDH mutant Gliomas have significantly higher DLL3 RNA (P<1x10-15) and protein by immunohistochemistry (P=0.0014 and P<4.3x10-6 in the discovery and validation set, respectively). DLL3 immunostaining was intense and homogeneous in IDH mutant Gliomas, retained in all recurrent tumors, and detected in only 1 of 20 non-tumor brains. Patient-derived IDH mutant Glioma tumorspheres overexpressed DLL3 and were potently sensitive to Rova-T in an antigen-dependent manner. Conclusions: DLL3 is selectively and homogeneously expressed in IDH mutant Gliomas and can be targeted with Rova-T in patient-derived IDH mutant Glioma tumorspheres. Our findings are potentially immediately translatable and have implications for therapeutic strategies that exploit cell surface tumor-associated antigens.
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Cell Surface Notch Ligand DLL3 is a Therapeutic Target in Isocitrate Dehydrogenase-mutant Glioma
Clinical Cancer Research, 2018Co-Authors: Marissa Spino, Sylvia C. Kurz, Luis Chiriboga, Jonathan Serrano, Briana Zeck, Namita Sen, Seema Patel, Guomiao Shen, Varshini Vasudevaraja, Aristotelis TsirigosAbstract:Purpose: Isocitrate dehydrogenase (IDH) mutant Gliomas are a distinct Glioma molecular subtype for which no effective molecularly-directed therapy exists. Low-grade Gliomas, which are 80-90% IDH mutant, have high RNA levels of the cell surface Notch ligand DLL3. We sought to determine DLL3 expression by immunohistochemistry in Glioma molecular subtypes and the potential efficacy of an anti-DLL3 antibody drug conjugate (ADC), rovalpituzumab tesirine (Rova-T), in IDH mutant Glioma. Experimental Design: We evaluated DLL3 expression by RNA using TCGA data and by immunohistochemistry in a discovery set of 63 Gliomas and 20 non-tumor brain tissues and a validation set of 62 known IDH wildtype and mutant Gliomas using a monoclonal anti-DLL3 antibody. Genotype was determined using a DNA methylation array classifier or by sequencing. The effect of Rova-T on patient-derived endogenous IDH mutant Glioma tumorspheres was determined by cell viability assay. Results: Compared to IDH wildtype glioblastoma, IDH mutant Gliomas have significantly higher DLL3 RNA (P
Di Wang - One of the best experts on this subject based on the ideXlab platform.
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knockdown of usf1 inhibits the vasculogenic mimicry of Glioma cells via stimulating snhg16 mir 212 3p and linc00667 mir 429 axis
Molecular therapy. Nucleic acids, 2019Co-Authors: Di Wang, Jian Zheng, Xiaobai Liu, Yixue Xue, Libo Liu, Heng Cai, Yunhui LiuAbstract:The anti-angiogenic treatment of malignant Glioma cells is an effective method to treat high-grade Gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of Gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in Gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in Glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in Glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of Glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of Glioma cells, and these findings might provide a novel strategy for Glioma treatment.
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Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis.
Molecular therapy. Nucleic acids, 2019Co-Authors: Di Wang, Jian Zheng, Xiaobai Liu, Yixue Xue, Libo Liu, Heng Cai, Yunhui LiuAbstract:The anti-angiogenic treatment of malignant Glioma cells is an effective method to treat high-grade Gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of Gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in Gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in Glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in Glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of Glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of Glioma cells, and these findings might provide a novel strategy for Glioma treatment.
Yixue Xue - One of the best experts on this subject based on the ideXlab platform.
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knockdown of usf1 inhibits the vasculogenic mimicry of Glioma cells via stimulating snhg16 mir 212 3p and linc00667 mir 429 axis
Molecular therapy. Nucleic acids, 2019Co-Authors: Di Wang, Jian Zheng, Xiaobai Liu, Yixue Xue, Libo Liu, Heng Cai, Yunhui LiuAbstract:The anti-angiogenic treatment of malignant Glioma cells is an effective method to treat high-grade Gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of Gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in Gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in Glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in Glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of Glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of Glioma cells, and these findings might provide a novel strategy for Glioma treatment.
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Knockdown of USF1 Inhibits the Vasculogenic Mimicry of Glioma Cells via Stimulating SNHG16/miR-212-3p and linc00667/miR-429 Axis.
Molecular therapy. Nucleic acids, 2019Co-Authors: Di Wang, Jian Zheng, Xiaobai Liu, Yixue Xue, Libo Liu, Heng Cai, Yunhui LiuAbstract:The anti-angiogenic treatment of malignant Glioma cells is an effective method to treat high-grade Gliomas. However, due to the presence of vasculogenic mimicry (VM), the anti-angiogenic treatment of Gliomas is not significantly effective in improving overall patient median survival. Therefore, this study investigated the mechanism of mimic formation of angiogenesis in Gliomas. The results of this experiment indicate that the expression of upstream transcription factor 1 (USF1) is upregulated in Glioma tissues and cells. USF1 knockdown inhibits the proliferation, migration, invasion, VM, and expression of VM-associated proteins in Glioma cells by stimulating SNHG16 and linc00667. These two long non-coding RNAs (lncRNAs) regulate ALHD1A1 through the competing endogenous RNA (ceRNA) mechanism influencing the VM of Glioma. This study is the first to demonstrate that the USF1/SNHG16/miR-212-3p/ALDH1A1 (aldehyde dehydrogenase-1) and USF1/linc00667/miR-429/ALDH1A1 axis regulates the VM of Glioma cells, and these findings might provide a novel strategy for Glioma treatment.
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Study of correlation between expression of bradykinin B2 receptor and pathological grade in human Gliomas
British journal of neurosurgery, 2005Co-Authors: Yi-song Zhao, Yixue Xue, Yunhui Liu, Nai-jia Jiang, Ping Wang, Zhi-hang Yang, Yuqin WangAbstract:In clinical practice there is a difference in response of the blood-tumour barrier (BTB) permeability induced by bradykinin in brain tumours with the same pathology. The variability in response of tumours to bradykinin is likely to be related to the expression level of bradykinin B2 receptor. This study used fresh human Glioma samples to determine the expression level of bradykinin B2 receptor on Gliomas with different pathological grades. The grade of tumour was classified using the WHO classification. To determine the bradykinin B2 receptor expression level in Gliomas, Immunohistochemistry and Western blot methods were used. In 24 cases of Gliomas there were eight cases of WHO I Glioma, eight cases of WHO II Glioma and eight cases of WHO III Glioma. Both Western blot and immunohistochemistry showed bradykinin B2 receptors localized on tumour cells, whilst brain cells at the edge of the Glioma hardly expressed B2 receptor. There were significant differences of bradykinin B2 receptor expression level amon...
Marissa Spino - One of the best experts on this subject based on the ideXlab platform.
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cell surface notch ligand dll3 is a therapeutic target in isocitrate dehydrogenase mutant Glioma
Clinical Cancer Research, 2019Co-Authors: Marissa Spino, Sylvia C. Kurz, Luis Chiriboga, Jonathan Serrano, Briana Zeck, Namita Sen, Seema Patel, Guomiao Shen, Varshini Vasudevaraja, Aristotelis TsirigosAbstract:Purpose: Isocitrate dehydrogenase (IDH) mutant Gliomas are a distinct Glioma molecular subtype for which no effective molecularly-directed therapy exists. Low-grade Gliomas, which are 80-90% IDH mutant, have high RNA levels of the cell surface Notch ligand DLL3. We sought to determine DLL3 expression by immunohistochemistry in Glioma molecular subtypes and the potential efficacy of an anti-DLL3 antibody drug conjugate (ADC), rovalpituzumab tesirine (Rova-T), in IDH mutant Glioma. Experimental Design: We evaluated DLL3 expression by RNA using TCGA data and by immunohistochemistry in a discovery set of 63 Gliomas and 20 non-tumor brain tissues and a validation set of 62 known IDH wildtype and mutant Gliomas using a monoclonal anti-DLL3 antibody. Genotype was determined using a DNA methylation array classifier or by sequencing. The effect of Rova-T on patient-derived endogenous IDH mutant Glioma tumorspheres was determined by cell viability assay. Results: Compared to IDH wildtype glioblastoma, IDH mutant Gliomas have significantly higher DLL3 RNA (P<1x10-15) and protein by immunohistochemistry (P=0.0014 and P<4.3x10-6 in the discovery and validation set, respectively). DLL3 immunostaining was intense and homogeneous in IDH mutant Gliomas, retained in all recurrent tumors, and detected in only 1 of 20 non-tumor brains. Patient-derived IDH mutant Glioma tumorspheres overexpressed DLL3 and were potently sensitive to Rova-T in an antigen-dependent manner. Conclusions: DLL3 is selectively and homogeneously expressed in IDH mutant Gliomas and can be targeted with Rova-T in patient-derived IDH mutant Glioma tumorspheres. Our findings are potentially immediately translatable and have implications for therapeutic strategies that exploit cell surface tumor-associated antigens.
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Cell Surface Notch Ligand DLL3 is a Therapeutic Target in Isocitrate Dehydrogenase-mutant Glioma
Clinical Cancer Research, 2018Co-Authors: Marissa Spino, Sylvia C. Kurz, Luis Chiriboga, Jonathan Serrano, Briana Zeck, Namita Sen, Seema Patel, Guomiao Shen, Varshini Vasudevaraja, Aristotelis TsirigosAbstract:Purpose: Isocitrate dehydrogenase (IDH) mutant Gliomas are a distinct Glioma molecular subtype for which no effective molecularly-directed therapy exists. Low-grade Gliomas, which are 80-90% IDH mutant, have high RNA levels of the cell surface Notch ligand DLL3. We sought to determine DLL3 expression by immunohistochemistry in Glioma molecular subtypes and the potential efficacy of an anti-DLL3 antibody drug conjugate (ADC), rovalpituzumab tesirine (Rova-T), in IDH mutant Glioma. Experimental Design: We evaluated DLL3 expression by RNA using TCGA data and by immunohistochemistry in a discovery set of 63 Gliomas and 20 non-tumor brain tissues and a validation set of 62 known IDH wildtype and mutant Gliomas using a monoclonal anti-DLL3 antibody. Genotype was determined using a DNA methylation array classifier or by sequencing. The effect of Rova-T on patient-derived endogenous IDH mutant Glioma tumorspheres was determined by cell viability assay. Results: Compared to IDH wildtype glioblastoma, IDH mutant Gliomas have significantly higher DLL3 RNA (P
