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
Autor*in: |
Fountas, Athanasios [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2015transfer abstract |
---|
Schlagwörter: |
---|
Umfang: |
14 |
---|
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.] |
---|---|
Übergeordnetes Werk: |
volume:26 ; year:2015 ; number:11 ; pages:643-656 ; extent:14 |
Links: |
---|
DOI / URN: |
10.1016/j.tem.2015.09.003 |
---|
Katalog-ID: |
ELV039856984 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | ELV039856984 | ||
003 | DE-627 | ||
005 | 20230625230109.0 | ||
007 | cr uuu---uuuuu | ||
008 | 180603s2015 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1016/j.tem.2015.09.003 |2 doi | |
028 | 5 | 2 | |a GBV00000000000147A.pica |
035 | |a (DE-627)ELV039856984 | ||
035 | |a (ELSEVIER)S1043-2760(15)00177-0 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
082 | 0 | |a 610 | |
082 | 0 | 4 | |a 610 |q DE-600 |
082 | 0 | 4 | |a 610 |q VZ |
084 | |a 44.90 |2 bkl | ||
100 | 1 | |a Fountas, Athanasios |e verfasserin |4 aut | |
245 | 1 | 0 | |a Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
264 | 1 | |c 2015transfer abstract | |
300 | |a 14 | ||
336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
337 | |a nicht spezifiziert |b z |2 rdamedia | ||
338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
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. | ||
650 | 7 | |a tyrosine kinase inhibitors |2 Elsevier | |
650 | 7 | |a PDGFR |2 Elsevier | |
650 | 7 | |a VEGFR |2 Elsevier | |
650 | 7 | |a c-Abl |2 Elsevier | |
650 | 7 | |a diabetes mellitus |2 Elsevier | |
650 | 7 | |a EGFR |2 Elsevier | |
700 | 1 | |a Diamantopoulos, Leonidas-Nikolaos |4 oth | |
700 | 1 | |a Tsatsoulis, Agathocles |4 oth | |
773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a van Egmond, L.T. ELSEVIER |t The gaze of sleep loss: acute effects of sleep loss on facial perception |d 2022 |g Amsterdam [u.a.] |w (DE-627)ELV008220654 |
773 | 1 | 8 | |g volume:26 |g year:2015 |g number:11 |g pages:643-656 |g extent:14 |
856 | 4 | 0 | |u https://doi.org/10.1016/j.tem.2015.09.003 |3 Volltext |
912 | |a GBV_USEFLAG_U | ||
912 | |a GBV_ELV | ||
912 | |a SYSFLAG_U | ||
912 | |a SSG-OLC-PHA | ||
936 | b | k | |a 44.90 |j Neurologie |q VZ |
951 | |a AR | ||
952 | |d 26 |j 2015 |e 11 |h 643-656 |g 14 | ||
953 | |2 045F |a 610 |
author_variant |
a f af |
---|---|
matchkey_str |
fountasathanasiosdiamantopoulosleonidasn:2015----:yoieiaeniiosndaeeaoet |
hierarchy_sort_str |
2015transfer abstract |
bklnumber |
44.90 |
publishDate |
2015 |
allfields |
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 |
spelling |
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 |
allfields_unstemmed |
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 |
allfieldsGer |
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 |
allfieldsSound |
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 |
language |
English |
source |
Enthalten in The gaze of sleep loss: acute effects of sleep loss on facial perception Amsterdam [u.a.] volume:26 year:2015 number:11 pages:643-656 extent:14 |
sourceStr |
Enthalten in The gaze of sleep loss: acute effects of sleep loss on facial perception Amsterdam [u.a.] volume:26 year:2015 number:11 pages:643-656 extent:14 |
format_phy_str_mv |
Article |
bklname |
Neurologie |
institution |
findex.gbv.de |
topic_facet |
tyrosine kinase inhibitors PDGFR VEGFR c-Abl diabetes mellitus EGFR |
dewey-raw |
610 |
isfreeaccess_bool |
false |
container_title |
The gaze of sleep loss: acute effects of sleep loss on facial perception |
authorswithroles_txt_mv |
Fountas, Athanasios @@aut@@ Diamantopoulos, Leonidas-Nikolaos @@oth@@ Tsatsoulis, Agathocles @@oth@@ |
publishDateDaySort_date |
2015-01-01T00:00:00Z |
hierarchy_top_id |
ELV008220654 |
dewey-sort |
3610 |
id |
ELV039856984 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV039856984</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625230109.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.tem.2015.09.003</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000147A.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV039856984</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1043-2760(15)00177-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Fountas, Athanasios</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm?</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">14</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">tyrosine kinase inhibitors</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PDGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">VEGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">c-Abl</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">diabetes mellitus</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Diamantopoulos, Leonidas-Nikolaos</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tsatsoulis, Agathocles</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">van Egmond, L.T. ELSEVIER</subfield><subfield code="t">The gaze of sleep loss: acute effects of sleep loss on facial perception</subfield><subfield code="d">2022</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV008220654</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:26</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:11</subfield><subfield code="g">pages:643-656</subfield><subfield code="g">extent:14</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.tem.2015.09.003</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.90</subfield><subfield code="j">Neurologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">26</subfield><subfield code="j">2015</subfield><subfield code="e">11</subfield><subfield code="h">643-656</subfield><subfield code="g">14</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
author |
Fountas, Athanasios |
spellingShingle |
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? |
authorStr |
Fountas, Athanasios |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV008220654 |
format |
electronic Article |
dewey-ones |
610 - Medicine & health |
delete_txt_mv |
keep |
author_role |
aut |
collection |
elsevier |
remote_str |
true |
illustrated |
Not Illustrated |
topic_title |
610 610 DE-600 610 VZ 44.90 bkl Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR Elsevier |
topic |
ddc 610 bkl 44.90 Elsevier tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR |
topic_unstemmed |
ddc 610 bkl 44.90 Elsevier tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR |
topic_browse |
ddc 610 bkl 44.90 Elsevier tyrosine kinase inhibitors Elsevier PDGFR Elsevier VEGFR Elsevier c-Abl Elsevier diabetes mellitus Elsevier EGFR |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
zu |
author2_variant |
l n d lnd a t at |
hierarchy_parent_title |
The gaze of sleep loss: acute effects of sleep loss on facial perception |
hierarchy_parent_id |
ELV008220654 |
dewey-tens |
610 - Medicine & health |
hierarchy_top_title |
The gaze of sleep loss: acute effects of sleep loss on facial perception |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)ELV008220654 |
title |
Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
ctrlnum |
(DE-627)ELV039856984 (ELSEVIER)S1043-2760(15)00177-0 |
title_full |
Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
author_sort |
Fountas, Athanasios |
journal |
The gaze of sleep loss: acute effects of sleep loss on facial perception |
journalStr |
The gaze of sleep loss: acute effects of sleep loss on facial perception |
lang_code |
eng |
isOA_bool |
false |
dewey-hundreds |
600 - Technology |
recordtype |
marc |
publishDateSort |
2015 |
contenttype_str_mv |
zzz |
container_start_page |
643 |
author_browse |
Fountas, Athanasios |
container_volume |
26 |
physical |
14 |
class |
610 610 DE-600 610 VZ 44.90 bkl |
format_se |
Elektronische Aufsätze |
author-letter |
Fountas, Athanasios |
doi_str_mv |
10.1016/j.tem.2015.09.003 |
dewey-full |
610 |
title_sort |
tyrosine kinase inhibitors and diabetes: a novel treatment paradigm? |
title_auth |
Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
abstract |
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. |
abstractGer |
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. |
abstract_unstemmed |
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. |
collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
container_issue |
11 |
title_short |
Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm? |
url |
https://doi.org/10.1016/j.tem.2015.09.003 |
remote_bool |
true |
author2 |
Diamantopoulos, Leonidas-Nikolaos Tsatsoulis, Agathocles |
author2Str |
Diamantopoulos, Leonidas-Nikolaos Tsatsoulis, Agathocles |
ppnlink |
ELV008220654 |
mediatype_str_mv |
z |
isOA_txt |
false |
hochschulschrift_bool |
false |
author2_role |
oth oth |
doi_str |
10.1016/j.tem.2015.09.003 |
up_date |
2024-07-06T21:40:13.288Z |
_version_ |
1803867403886526464 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV039856984</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625230109.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.tem.2015.09.003</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000147A.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV039856984</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1043-2760(15)00177-0</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Fountas, Athanasios</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Tyrosine Kinase Inhibitors and Diabetes: A Novel Treatment Paradigm?</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">14</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="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.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">tyrosine kinase inhibitors</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PDGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">VEGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">c-Abl</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">diabetes mellitus</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">EGFR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Diamantopoulos, Leonidas-Nikolaos</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tsatsoulis, Agathocles</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">van Egmond, L.T. ELSEVIER</subfield><subfield code="t">The gaze of sleep loss: acute effects of sleep loss on facial perception</subfield><subfield code="d">2022</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV008220654</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:26</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:11</subfield><subfield code="g">pages:643-656</subfield><subfield code="g">extent:14</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.tem.2015.09.003</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.90</subfield><subfield code="j">Neurologie</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">26</subfield><subfield code="j">2015</subfield><subfield code="e">11</subfield><subfield code="h">643-656</subfield><subfield code="g">14</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
score |
7.401186 |