The Experts below are selected from a list of 9 Experts worldwide ranked by ideXlab platform
Daniela De Martino - One of the best experts on this subject based on the ideXlab platform.
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the Quassinoid Derivative nbt 272 targets both the akt and erk signaling pathways in embryonal tumors
Molecular Cancer Therapeutics, 2010Co-Authors: Deborah Castelletti, Giulio Fiaschetti, Valeria Di Dato, Urs Ziegler, Candy Kumps, Katleen De Preter, Massimo Zollo, Franki Speleman, Tarek Shalaby, Daniela De MartinoAbstract:The Quassinoid analogue NBT-272 has been reported to inhibit MYC, thus warranting a further effort to better understand its preclinical properties in models of embryonal tumors (ET), a family of childhood malignancies sharing relevant biological and genetic features such as deregulated expression of MYC oncogenes. In our study, NBT-272 displayed a strong anti-proliferative activity in vitro that resulted from the combination of diverse biological effects, ranging from G1/S arrest of the cell cycle to apoptosis and autophagy. The compound prevented the full activation of both the eukaryotic initiation factor 4E (eIF4E) and its binding protein 4EBP-1, regulating cap-dependent protein translation. Interestingly, all responses induced by NBT-272 in ET could be attributed to interference with two main pro-proliferative signaling pathways, i.e. the AKT and the MEK/extracellular signal-regulated kinase (ERK) pathways. These findings also suggested that the depleting effect of NBT-272 on MYC protein expression occurred via indirect mechanisms, rather than selective inhibition. Finally, the ability of NBT-272 to arrest tumor growth in a xenograft model of neuroblastoma plays a role in the strong anti-tumor activity of this compound, both in vitro and in vivo, with its potential to target cell-survival pathways that are relevant for the development and progression of ET.
Deborah Castelletti - One of the best experts on this subject based on the ideXlab platform.
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the Quassinoid Derivative nbt 272 targets both the akt and erk signaling pathways in embryonal tumors
Molecular Cancer Therapeutics, 2010Co-Authors: Deborah Castelletti, Giulio Fiaschetti, Valeria Di Dato, Urs Ziegler, Candy Kumps, Katleen De Preter, Massimo Zollo, Franki Speleman, Tarek Shalaby, Daniela De MartinoAbstract:The Quassinoid analogue NBT-272 has been reported to inhibit MYC, thus warranting a further effort to better understand its preclinical properties in models of embryonal tumors (ET), a family of childhood malignancies sharing relevant biological and genetic features such as deregulated expression of MYC oncogenes. In our study, NBT-272 displayed a strong anti-proliferative activity in vitro that resulted from the combination of diverse biological effects, ranging from G1/S arrest of the cell cycle to apoptosis and autophagy. The compound prevented the full activation of both the eukaryotic initiation factor 4E (eIF4E) and its binding protein 4EBP-1, regulating cap-dependent protein translation. Interestingly, all responses induced by NBT-272 in ET could be attributed to interference with two main pro-proliferative signaling pathways, i.e. the AKT and the MEK/extracellular signal-regulated kinase (ERK) pathways. These findings also suggested that the depleting effect of NBT-272 on MYC protein expression occurred via indirect mechanisms, rather than selective inhibition. Finally, the ability of NBT-272 to arrest tumor growth in a xenograft model of neuroblastoma plays a role in the strong anti-tumor activity of this compound, both in vitro and in vivo, with its potential to target cell-survival pathways that are relevant for the development and progression of ET.
Valeria Di Dato - One of the best experts on this subject based on the ideXlab platform.
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the Quassinoid Derivative nbt 272 targets both the akt and erk signaling pathways in embryonal tumors
Molecular Cancer Therapeutics, 2010Co-Authors: Deborah Castelletti, Giulio Fiaschetti, Valeria Di Dato, Urs Ziegler, Candy Kumps, Katleen De Preter, Massimo Zollo, Franki Speleman, Tarek Shalaby, Daniela De MartinoAbstract:The Quassinoid analogue NBT-272 has been reported to inhibit MYC, thus warranting a further effort to better understand its preclinical properties in models of embryonal tumors (ET), a family of childhood malignancies sharing relevant biological and genetic features such as deregulated expression of MYC oncogenes. In our study, NBT-272 displayed a strong anti-proliferative activity in vitro that resulted from the combination of diverse biological effects, ranging from G1/S arrest of the cell cycle to apoptosis and autophagy. The compound prevented the full activation of both the eukaryotic initiation factor 4E (eIF4E) and its binding protein 4EBP-1, regulating cap-dependent protein translation. Interestingly, all responses induced by NBT-272 in ET could be attributed to interference with two main pro-proliferative signaling pathways, i.e. the AKT and the MEK/extracellular signal-regulated kinase (ERK) pathways. These findings also suggested that the depleting effect of NBT-272 on MYC protein expression occurred via indirect mechanisms, rather than selective inhibition. Finally, the ability of NBT-272 to arrest tumor growth in a xenograft model of neuroblastoma plays a role in the strong anti-tumor activity of this compound, both in vitro and in vivo, with its potential to target cell-survival pathways that are relevant for the development and progression of ET.
Tarek Shalaby - One of the best experts on this subject based on the ideXlab platform.
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the Quassinoid Derivative nbt 272 targets both the akt and erk signaling pathways in embryonal tumors
Molecular Cancer Therapeutics, 2010Co-Authors: Deborah Castelletti, Giulio Fiaschetti, Valeria Di Dato, Urs Ziegler, Candy Kumps, Katleen De Preter, Massimo Zollo, Franki Speleman, Tarek Shalaby, Daniela De MartinoAbstract:The Quassinoid analogue NBT-272 has been reported to inhibit MYC, thus warranting a further effort to better understand its preclinical properties in models of embryonal tumors (ET), a family of childhood malignancies sharing relevant biological and genetic features such as deregulated expression of MYC oncogenes. In our study, NBT-272 displayed a strong anti-proliferative activity in vitro that resulted from the combination of diverse biological effects, ranging from G1/S arrest of the cell cycle to apoptosis and autophagy. The compound prevented the full activation of both the eukaryotic initiation factor 4E (eIF4E) and its binding protein 4EBP-1, regulating cap-dependent protein translation. Interestingly, all responses induced by NBT-272 in ET could be attributed to interference with two main pro-proliferative signaling pathways, i.e. the AKT and the MEK/extracellular signal-regulated kinase (ERK) pathways. These findings also suggested that the depleting effect of NBT-272 on MYC protein expression occurred via indirect mechanisms, rather than selective inhibition. Finally, the ability of NBT-272 to arrest tumor growth in a xenograft model of neuroblastoma plays a role in the strong anti-tumor activity of this compound, both in vitro and in vivo, with its potential to target cell-survival pathways that are relevant for the development and progression of ET.
Franki Speleman - One of the best experts on this subject based on the ideXlab platform.
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the Quassinoid Derivative nbt 272 targets both the akt and erk signaling pathways in embryonal tumors
Molecular Cancer Therapeutics, 2010Co-Authors: Deborah Castelletti, Giulio Fiaschetti, Valeria Di Dato, Urs Ziegler, Candy Kumps, Katleen De Preter, Massimo Zollo, Franki Speleman, Tarek Shalaby, Daniela De MartinoAbstract:The Quassinoid analogue NBT-272 has been reported to inhibit MYC, thus warranting a further effort to better understand its preclinical properties in models of embryonal tumors (ET), a family of childhood malignancies sharing relevant biological and genetic features such as deregulated expression of MYC oncogenes. In our study, NBT-272 displayed a strong anti-proliferative activity in vitro that resulted from the combination of diverse biological effects, ranging from G1/S arrest of the cell cycle to apoptosis and autophagy. The compound prevented the full activation of both the eukaryotic initiation factor 4E (eIF4E) and its binding protein 4EBP-1, regulating cap-dependent protein translation. Interestingly, all responses induced by NBT-272 in ET could be attributed to interference with two main pro-proliferative signaling pathways, i.e. the AKT and the MEK/extracellular signal-regulated kinase (ERK) pathways. These findings also suggested that the depleting effect of NBT-272 on MYC protein expression occurred via indirect mechanisms, rather than selective inhibition. Finally, the ability of NBT-272 to arrest tumor growth in a xenograft model of neuroblastoma plays a role in the strong anti-tumor activity of this compound, both in vitro and in vivo, with its potential to target cell-survival pathways that are relevant for the development and progression of ET.
