Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm?
Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes m...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Fountas, Athanasios [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
14 |
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| Übergeordnetes Werk: |
Enthalten in: The gaze of sleep loss: acute effects of sleep loss on facial perception - van Egmond, L.T. ELSEVIER, 2022, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:26 ; year:2015 ; number:11 ; pages:643-656 ; extent:14 |
| Links: |
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| DOI / URN: |
10.1016/j.tem.2015.09.003 |
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| 520 | |a Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. | ||
| 520 | |a Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. | ||
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10.1016/j.tem.2015.09.003 doi GBV00000000000147A.pica (DE-627)ELV039856984 (ELSEVIER)S1043-2760(15)00177-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.90 bkl Fountas, Athanasios verfasserin aut Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? 2015transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Elsevier Diamantopoulos, Leonidas-Nikolaos oth Tsatsoulis, Agathocles oth Enthalten in Elsevier Science van Egmond, L.T. ELSEVIER The gaze of sleep loss: acute effects of sleep loss on facial perception 2022 Amsterdam [u.a.] (DE-627)ELV008220654 volume:26 year:2015 number:11 pages:643-656 extent:14 https://doi.org/10.1016/j.tem.2015.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.90 Neurologie VZ AR 26 2015 11 643-656 14 045F 610 |
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10.1016/j.tem.2015.09.003 doi GBV00000000000147A.pica (DE-627)ELV039856984 (ELSEVIER)S1043-2760(15)00177-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.90 bkl Fountas, Athanasios verfasserin aut Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? 2015transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Elsevier Diamantopoulos, Leonidas-Nikolaos oth Tsatsoulis, Agathocles oth Enthalten in Elsevier Science van Egmond, L.T. ELSEVIER The gaze of sleep loss: acute effects of sleep loss on facial perception 2022 Amsterdam [u.a.] (DE-627)ELV008220654 volume:26 year:2015 number:11 pages:643-656 extent:14 https://doi.org/10.1016/j.tem.2015.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.90 Neurologie VZ AR 26 2015 11 643-656 14 045F 610 |
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10.1016/j.tem.2015.09.003 doi GBV00000000000147A.pica (DE-627)ELV039856984 (ELSEVIER)S1043-2760(15)00177-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.90 bkl Fountas, Athanasios verfasserin aut Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? 2015transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Elsevier Diamantopoulos, Leonidas-Nikolaos oth Tsatsoulis, Agathocles oth Enthalten in Elsevier Science van Egmond, L.T. ELSEVIER The gaze of sleep loss: acute effects of sleep loss on facial perception 2022 Amsterdam [u.a.] (DE-627)ELV008220654 volume:26 year:2015 number:11 pages:643-656 extent:14 https://doi.org/10.1016/j.tem.2015.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.90 Neurologie VZ AR 26 2015 11 643-656 14 045F 610 |
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10.1016/j.tem.2015.09.003 doi GBV00000000000147A.pica (DE-627)ELV039856984 (ELSEVIER)S1043-2760(15)00177-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.90 bkl Fountas, Athanasios verfasserin aut Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? 2015transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Elsevier Diamantopoulos, Leonidas-Nikolaos oth Tsatsoulis, Agathocles oth Enthalten in Elsevier Science van Egmond, L.T. ELSEVIER The gaze of sleep loss: acute effects of sleep loss on facial perception 2022 Amsterdam [u.a.] (DE-627)ELV008220654 volume:26 year:2015 number:11 pages:643-656 extent:14 https://doi.org/10.1016/j.tem.2015.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.90 Neurologie VZ AR 26 2015 11 643-656 14 045F 610 |
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10.1016/j.tem.2015.09.003 doi GBV00000000000147A.pica (DE-627)ELV039856984 (ELSEVIER)S1043-2760(15)00177-0 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.90 bkl Fountas, Athanasios verfasserin aut Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? 2015transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Elsevier Diamantopoulos, Leonidas-Nikolaos oth Tsatsoulis, Agathocles oth Enthalten in Elsevier Science van Egmond, L.T. ELSEVIER The gaze of sleep loss: acute effects of sleep loss on facial perception 2022 Amsterdam [u.a.] (DE-627)ELV008220654 volume:26 year:2015 number:11 pages:643-656 extent:14 https://doi.org/10.1016/j.tem.2015.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.90 Neurologie VZ AR 26 2015 11 643-656 14 045F 610 |
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Fountas, Athanasios |
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Fountas, Athanasios ddc 610 bkl 44.90 Elsevier tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
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Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
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Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. |
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Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. |
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Deregulation of protein tyrosine kinase (PTK) activity is implicated in various proliferative conditions. Multi-target tyrosine kinase inhibitors (TKIs) are increasingly used for the treatment of different malignancies. Recently, several clinical cases of the reversal of both type 1 and 2 diabetes mellitus (T1DM, T2DM) during TKI administration have been reported. Experimental in vivo and in vitro studies have elucidated some of the mechanisms behind this effect. For example, inhibition of Abelson tyrosine kinase (c-Abl) results in β cell survival and enhanced insulin secretion, while platelet-derived growth factor receptor (PDGFR) and epidermal growth factor receptor (EGFR) inhibition leads to improvement in insulin sensitivity. In addition, inhibition of vascular endothelial growth factor receptor 2 (VEGFR2) reduces the degree of islet cell inflammation (insulitis). Therefore, targeting several PTKs may provide a novel approach for correcting the pathophysiologic disturbances of diabetes. |
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