The Experts below are selected from a list of 12108 Experts worldwide ranked by ideXlab platform

Sílvia Cufí - One of the best experts on this subject based on the ideXlab platform.

  • Silibinin suppresses EMT-driven Erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Alejandro Vazquez-martin, Bruna Corominas-faja, Cristina Oliveras-ferraros, Elisabet Cuyàs, Begoña Martin-castillo, Enrique Barrajón-catalán, Joana Visa, Antonio Segura-carretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21 /low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL , ZEB and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

  • silibinin suppresses emt driven Erlotinib resistance by reversing the high mir 21 low mir 200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Elisabet Cuyàs, Joana Visa, Alejandro Vazquezmartin, Cristina Oliverasferraros, Bruna Corominasfaja, Begona Martincastillo, Enrique Barrajoncatalan, Antonio Seguracarretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21/low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL, ZEB, and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

Antonio Seguracarretero - One of the best experts on this subject based on the ideXlab platform.

  • silibinin suppresses emt driven Erlotinib resistance by reversing the high mir 21 low mir 200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Elisabet Cuyàs, Joana Visa, Alejandro Vazquezmartin, Cristina Oliverasferraros, Bruna Corominasfaja, Begona Martincastillo, Enrique Barrajoncatalan, Antonio Seguracarretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21/low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL, ZEB, and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

Antonio Segura-carretero - One of the best experts on this subject based on the ideXlab platform.

  • Silibinin suppresses EMT-driven Erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Alejandro Vazquez-martin, Bruna Corominas-faja, Cristina Oliveras-ferraros, Elisabet Cuyàs, Begoña Martin-castillo, Enrique Barrajón-catalán, Joana Visa, Antonio Segura-carretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21 /low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL , ZEB and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

Rosa Bonavia - One of the best experts on this subject based on the ideXlab platform.

  • Silibinin suppresses EMT-driven Erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Alejandro Vazquez-martin, Bruna Corominas-faja, Cristina Oliveras-ferraros, Elisabet Cuyàs, Begoña Martin-castillo, Enrique Barrajón-catalán, Joana Visa, Antonio Segura-carretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21 /low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL , ZEB and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

  • silibinin suppresses emt driven Erlotinib resistance by reversing the high mir 21 low mir 200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Elisabet Cuyàs, Joana Visa, Alejandro Vazquezmartin, Cristina Oliverasferraros, Bruna Corominasfaja, Begona Martincastillo, Enrique Barrajoncatalan, Antonio Seguracarretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21/low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL, ZEB, and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

Joana Visa - One of the best experts on this subject based on the ideXlab platform.

  • Silibinin suppresses EMT-driven Erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Alejandro Vazquez-martin, Bruna Corominas-faja, Cristina Oliveras-ferraros, Elisabet Cuyàs, Begoña Martin-castillo, Enrique Barrajón-catalán, Joana Visa, Antonio Segura-carretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21 /low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL , ZEB and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.

  • silibinin suppresses emt driven Erlotinib resistance by reversing the high mir 21 low mir 200c signature in vivo
    Scientific Reports, 2013
    Co-Authors: Sílvia Cufí, Rosa Bonavia, Elisabet Cuyàs, Joana Visa, Alejandro Vazquezmartin, Cristina Oliverasferraros, Bruna Corominasfaja, Begona Martincastillo, Enrique Barrajoncatalan, Antonio Seguracarretero
    Abstract:

    The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to Erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of Erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of Erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21/low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL, ZEB, and N-cadherin observed in Erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in Erlotinib-refractory cells and prevent the highly migratogenic phenotype of Erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to Erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following Erlotinib treatment.