<i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas

<i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the me...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Maximilian Scheer [verfasserIn] Sandra Leisz [verfasserIn] Eberhard Sorge [verfasserIn] Olha Storozhuk [verfasserIn] Julian Prell [verfasserIn] Ivy Ho [verfasserIn] Anja Harder [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	glioblastoma neurofibromatosis NF1 neurofibromin mesenchymal invasiveness

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 23(2021), 1, p 352
Übergeordnetes Werk:	volume:23 ; year:2021 ; number:1, p 352

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms23010352

Katalog-ID:	DOAJ087069261

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Indexfelder

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allfields	10.3390/ijms23010352 doi (DE-627)DOAJ087069261 (DE-599)DOAJcc6807f6b58c4c1081b03c97cf475eb4 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Maximilian Scheer verfasserin aut <i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review. glioblastoma neurofibromatosis NF1 neurofibromin mesenchymal invasiveness Biology (General) Chemistry Sandra Leisz verfasserin aut Eberhard Sorge verfasserin aut Olha Storozhuk verfasserin aut Julian Prell verfasserin aut Ivy Ho verfasserin aut Anja Harder verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2021), 1, p 352 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2021 number:1, p 352 https://doi.org/10.3390/ijms23010352 kostenfrei https://doaj.org/article/cc6807f6b58c4c1081b03c97cf475eb4 kostenfrei https://www.mdpi.com/1422-0067/23/1/352 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2021 1, p 352
spelling	10.3390/ijms23010352 doi (DE-627)DOAJ087069261 (DE-599)DOAJcc6807f6b58c4c1081b03c97cf475eb4 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Maximilian Scheer verfasserin aut <i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review. glioblastoma neurofibromatosis NF1 neurofibromin mesenchymal invasiveness Biology (General) Chemistry Sandra Leisz verfasserin aut Eberhard Sorge verfasserin aut Olha Storozhuk verfasserin aut Julian Prell verfasserin aut Ivy Ho verfasserin aut Anja Harder verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2021), 1, p 352 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2021 number:1, p 352 https://doi.org/10.3390/ijms23010352 kostenfrei https://doaj.org/article/cc6807f6b58c4c1081b03c97cf475eb4 kostenfrei https://www.mdpi.com/1422-0067/23/1/352 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2021 1, p 352
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allfieldsGer	10.3390/ijms23010352 doi (DE-627)DOAJ087069261 (DE-599)DOAJcc6807f6b58c4c1081b03c97cf475eb4 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Maximilian Scheer verfasserin aut <i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review. glioblastoma neurofibromatosis NF1 neurofibromin mesenchymal invasiveness Biology (General) Chemistry Sandra Leisz verfasserin aut Eberhard Sorge verfasserin aut Olha Storozhuk verfasserin aut Julian Prell verfasserin aut Ivy Ho verfasserin aut Anja Harder verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2021), 1, p 352 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2021 number:1, p 352 https://doi.org/10.3390/ijms23010352 kostenfrei https://doaj.org/article/cc6807f6b58c4c1081b03c97cf475eb4 kostenfrei https://www.mdpi.com/1422-0067/23/1/352 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2021 1, p 352
allfieldsSound	10.3390/ijms23010352 doi (DE-627)DOAJ087069261 (DE-599)DOAJcc6807f6b58c4c1081b03c97cf475eb4 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Maximilian Scheer verfasserin aut <i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review. glioblastoma neurofibromatosis NF1 neurofibromin mesenchymal invasiveness Biology (General) Chemistry Sandra Leisz verfasserin aut Eberhard Sorge verfasserin aut Olha Storozhuk verfasserin aut Julian Prell verfasserin aut Ivy Ho verfasserin aut Anja Harder verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 23(2021), 1, p 352 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:23 year:2021 number:1, p 352 https://doi.org/10.3390/ijms23010352 kostenfrei https://doaj.org/article/cc6807f6b58c4c1081b03c97cf475eb4 kostenfrei https://www.mdpi.com/1422-0067/23/1/352 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 23 2021 1, p 352
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container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Maximilian Scheer @@aut@@ Sandra Leisz @@aut@@ Eberhard Sorge @@aut@@ Olha Storozhuk @@aut@@ Julian Prell @@aut@@ Ivy Ho @@aut@@ Anja Harder @@aut@@
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callnumber-first	Q - Science
author	Maximilian Scheer
spellingShingle	Maximilian Scheer misc QH301-705.5 misc QD1-999 misc glioblastoma misc neurofibromatosis misc NF1 misc neurofibromin misc mesenchymal misc invasiveness misc Biology (General) misc Chemistry <i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas
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topic_title	QH301-705.5 QD1-999 <i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas glioblastoma neurofibromatosis NF1 neurofibromin mesenchymal invasiveness
topic	misc QH301-705.5 misc QD1-999 misc glioblastoma misc neurofibromatosis misc NF1 misc neurofibromin misc mesenchymal misc invasiveness misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc glioblastoma misc neurofibromatosis misc NF1 misc neurofibromin misc mesenchymal misc invasiveness misc Biology (General) misc Chemistry
topic_browse	misc QH301-705.5 misc QD1-999 misc glioblastoma misc neurofibromatosis misc NF1 misc neurofibromin misc mesenchymal misc invasiveness misc Biology (General) misc Chemistry
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title	<i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas
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title_sort	<i<neurofibromatosis type 1</i< gene alterations define specific features of a subset of glioblastomas
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title_auth	<i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas
abstract	<i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review.
abstractGer	<i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review.
abstract_unstemmed	<i<Neurofibromatosis type 1</i< (<i<NF1</i<) gene mutations or alterations occur within neurofibromatosis type 1 as well as in many different malignant tumours on the somatic level. In glioblastoma, <i<NF1</i< loss of function plays a major role in inducing the mesenchymal (MES) subtype and, therefore defining the most aggressive glioblastoma. This is associated with an immune signature and mediated via the NF1–MAPK–FOSL1 axis. Specifically, increased invasion seems to be regulated via mutations in the leucine-rich domain (LRD) of the <i<NF1</i< gene product neurofibromin. Novel targets for therapy may arise from neurofibromin deficiency-associated cellular mechanisms that are summarised in this review.
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container_issue	1, p 352
title_short	<i<Neurofibromatosis Type 1</i< Gene Alterations Define Specific Features of a Subset of Glioblastomas
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