The Contribution of Oxidative Stress to <i<NF1</i<-Altered Tumors

The neurofibromatosis-1 gene (<i<NF1</i<) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Elisabetta Kuhn [verfasserIn] Federica Natacci [verfasserIn] Massimo Corbo [verfasserIn] Luigi Pisani [verfasserIn] Stefano Ferrero [verfasserIn] Gaetano Bulfamante [verfasserIn] Donatella Gambini [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	neurofibromatosis pathogenesis neurofibromin oxidative stress ROS

Übergeordnetes Werk:	In: Antioxidants - MDPI AG, 2013, 12(2023), 8, p 1557
Übergeordnetes Werk:	volume:12 ; year:2023 ; number:8, p 1557

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/antiox12081557

Katalog-ID:	DOAJ093658648

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520			\|a The neurofibromatosis-1 gene (<i<NF1</i<) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated <i<NF1</i< as one of the most frequently mutated genes in human cancer, being mutated in approximately 5–10% of all tumors, especially in malignant peripheral nerve sheath tumors and different skin tumors. <i<NF1</i< acts as a tumor suppressor gene that encodes neurofibromin, a large protein that controls neoplastic transformation through several molecular mechanisms. On the other hand, neurofibromin loss due to <i<NF1</i< biallelic inactivation induces tumorigenic hyperactivation of Ras and mTOR signaling pathways. Moreover, neurofibromin controls actin cytoskeleton structure and the metaphase–anaphase transition. Consequently, neurofibromin deficiency favors cell mobility and proliferation as well as chromosomal instability and aneuploidy, respectively. Growing evidence supports the role of oxidative stress in <i<NF1</i<-related tumorigenesis. Neurofibromin loss induces oxidative stress both directly and through Ras and mTOR signaling activation. Notably, innovative therapeutic approaches explore drug combinations that further increase reactive oxygen species to boost the oxidative unbalance of <i<NF1</i<-altered cancer cells. In our paper, we review <i<NF1</i<-related tumors and their pathogenesis, highlighting the twofold contribution of oxidative stress, both tumorigenic and therapeutic.
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allfieldsSound	10.3390/antiox12081557 doi (DE-627)DOAJ093658648 (DE-599)DOAJ8c04810aa30a4e849ba66ee866082b5b DE-627 ger DE-627 rakwb eng RM1-950 Elisabetta Kuhn verfasserin aut The Contribution of Oxidative Stress to <i<NF1</i<-Altered Tumors 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The neurofibromatosis-1 gene (<i<NF1</i<) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated <i<NF1</i< as one of the most frequently mutated genes in human cancer, being mutated in approximately 5–10% of all tumors, especially in malignant peripheral nerve sheath tumors and different skin tumors. <i<NF1</i< acts as a tumor suppressor gene that encodes neurofibromin, a large protein that controls neoplastic transformation through several molecular mechanisms. On the other hand, neurofibromin loss due to <i<NF1</i< biallelic inactivation induces tumorigenic hyperactivation of Ras and mTOR signaling pathways. Moreover, neurofibromin controls actin cytoskeleton structure and the metaphase–anaphase transition. Consequently, neurofibromin deficiency favors cell mobility and proliferation as well as chromosomal instability and aneuploidy, respectively. Growing evidence supports the role of oxidative stress in <i<NF1</i<-related tumorigenesis. Neurofibromin loss induces oxidative stress both directly and through Ras and mTOR signaling activation. Notably, innovative therapeutic approaches explore drug combinations that further increase reactive oxygen species to boost the oxidative unbalance of <i<NF1</i<-altered cancer cells. In our paper, we review <i<NF1</i<-related tumors and their pathogenesis, highlighting the twofold contribution of oxidative stress, both tumorigenic and therapeutic. neurofibromatosis <i<NF1</i< pathogenesis neurofibromin oxidative stress ROS Therapeutics. Pharmacology Federica Natacci verfasserin aut Massimo Corbo verfasserin aut Luigi Pisani verfasserin aut Stefano Ferrero verfasserin aut Gaetano Bulfamante verfasserin aut Donatella Gambini verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 8, p 1557 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:8, p 1557 https://doi.org/10.3390/antiox12081557 kostenfrei https://doaj.org/article/8c04810aa30a4e849ba66ee866082b5b kostenfrei https://www.mdpi.com/2076-3921/12/8/1557 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 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 12 2023 8, p 1557
language	English
source	In Antioxidants 12(2023), 8, p 1557 volume:12 year:2023 number:8, p 1557
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topic_facet	neurofibromatosis <i<NF1</i< pathogenesis neurofibromin oxidative stress ROS Therapeutics. Pharmacology
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container_title	Antioxidants
authorswithroles_txt_mv	Elisabetta Kuhn @@aut@@ Federica Natacci @@aut@@ Massimo Corbo @@aut@@ Luigi Pisani @@aut@@ Stefano Ferrero @@aut@@ Gaetano Bulfamante @@aut@@ Donatella Gambini @@aut@@
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callnumber-first	R - Medicine
author	Elisabetta Kuhn
spellingShingle	Elisabetta Kuhn misc RM1-950 misc neurofibromatosis misc <i<NF1</i< misc pathogenesis misc neurofibromin misc oxidative stress misc ROS misc Therapeutics. Pharmacology The Contribution of Oxidative Stress to <i<NF1</i<-Altered Tumors
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topic_title	RM1-950 The Contribution of Oxidative Stress to <i<NF1</i<-Altered Tumors neurofibromatosis <i<NF1</i< pathogenesis neurofibromin oxidative stress ROS
topic	misc RM1-950 misc neurofibromatosis misc <i<NF1</i< misc pathogenesis misc neurofibromin misc oxidative stress misc ROS misc Therapeutics. Pharmacology
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title_sort	contribution of oxidative stress to <i<nf1</i<-altered tumors
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title_auth	The Contribution of Oxidative Stress to <i<NF1</i<-Altered Tumors
abstract	The neurofibromatosis-1 gene (<i<NF1</i<) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated <i<NF1</i< as one of the most frequently mutated genes in human cancer, being mutated in approximately 5–10% of all tumors, especially in malignant peripheral nerve sheath tumors and different skin tumors. <i<NF1</i< acts as a tumor suppressor gene that encodes neurofibromin, a large protein that controls neoplastic transformation through several molecular mechanisms. On the other hand, neurofibromin loss due to <i<NF1</i< biallelic inactivation induces tumorigenic hyperactivation of Ras and mTOR signaling pathways. Moreover, neurofibromin controls actin cytoskeleton structure and the metaphase–anaphase transition. Consequently, neurofibromin deficiency favors cell mobility and proliferation as well as chromosomal instability and aneuploidy, respectively. Growing evidence supports the role of oxidative stress in <i<NF1</i<-related tumorigenesis. Neurofibromin loss induces oxidative stress both directly and through Ras and mTOR signaling activation. Notably, innovative therapeutic approaches explore drug combinations that further increase reactive oxygen species to boost the oxidative unbalance of <i<NF1</i<-altered cancer cells. In our paper, we review <i<NF1</i<-related tumors and their pathogenesis, highlighting the twofold contribution of oxidative stress, both tumorigenic and therapeutic.
abstractGer	The neurofibromatosis-1 gene (<i<NF1</i<) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated <i<NF1</i< as one of the most frequently mutated genes in human cancer, being mutated in approximately 5–10% of all tumors, especially in malignant peripheral nerve sheath tumors and different skin tumors. <i<NF1</i< acts as a tumor suppressor gene that encodes neurofibromin, a large protein that controls neoplastic transformation through several molecular mechanisms. On the other hand, neurofibromin loss due to <i<NF1</i< biallelic inactivation induces tumorigenic hyperactivation of Ras and mTOR signaling pathways. Moreover, neurofibromin controls actin cytoskeleton structure and the metaphase–anaphase transition. Consequently, neurofibromin deficiency favors cell mobility and proliferation as well as chromosomal instability and aneuploidy, respectively. Growing evidence supports the role of oxidative stress in <i<NF1</i<-related tumorigenesis. Neurofibromin loss induces oxidative stress both directly and through Ras and mTOR signaling activation. Notably, innovative therapeutic approaches explore drug combinations that further increase reactive oxygen species to boost the oxidative unbalance of <i<NF1</i<-altered cancer cells. In our paper, we review <i<NF1</i<-related tumors and their pathogenesis, highlighting the twofold contribution of oxidative stress, both tumorigenic and therapeutic.
abstract_unstemmed	The neurofibromatosis-1 gene (<i<NF1</i<) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated <i<NF1</i< as one of the most frequently mutated genes in human cancer, being mutated in approximately 5–10% of all tumors, especially in malignant peripheral nerve sheath tumors and different skin tumors. <i<NF1</i< acts as a tumor suppressor gene that encodes neurofibromin, a large protein that controls neoplastic transformation through several molecular mechanisms. On the other hand, neurofibromin loss due to <i<NF1</i< biallelic inactivation induces tumorigenic hyperactivation of Ras and mTOR signaling pathways. Moreover, neurofibromin controls actin cytoskeleton structure and the metaphase–anaphase transition. Consequently, neurofibromin deficiency favors cell mobility and proliferation as well as chromosomal instability and aneuploidy, respectively. Growing evidence supports the role of oxidative stress in <i<NF1</i<-related tumorigenesis. Neurofibromin loss induces oxidative stress both directly and through Ras and mTOR signaling activation. Notably, innovative therapeutic approaches explore drug combinations that further increase reactive oxygen species to boost the oxidative unbalance of <i<NF1</i<-altered cancer cells. In our paper, we review <i<NF1</i<-related tumors and their pathogenesis, highlighting the twofold contribution of oxidative stress, both tumorigenic and therapeutic.
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The Contribution of Oxidative Stress to <i<NF1</i<-Altered Tumors

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