PI3K抑制在胶质母细胞瘤和神经母细胞瘤治疗中的关键评价。

Molecular and cellular therapies Pub Date : 2014-10-27 eCollection Date: 2014-01-01
Mike-Andrew Westhoff, Georg Karpel-Massler, Oliver Brühl, Stefanie Enzenmüller, Katia La Ferla-Brühl, Markus D Siegelin, Lisa Nonnenmacher, Klaus-Michael Debatin
{"title":"PI3K抑制在胶质母细胞瘤和神经母细胞瘤治疗中的关键评价。","authors":"Mike-Andrew Westhoff, Georg Karpel-Massler, Oliver Brühl, Stefanie Enzenmüller, Katia La Ferla-Brühl, Markus D Siegelin, Lisa Nonnenmacher, Klaus-Michael Debatin","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Members of the PI3K/Akt/mTor signaling cascade are among the most frequently altered proteins in cancer, yet the therapeutic application of pharmacological inhibitors of this signaling network, either as monotherapy or in combination therapy (CT) has so far not been particularly successful. In this review we will focus on the role of PI3K/Akt/mTOR in two distinct tumors, Glioblastoma multiforme (GBM), an adult brain tumor which frequently exhibits PTEN inactivation, and Neuroblastoma (NB), a childhood malignancy that affects the central nervous system and does not harbor any classic alterations in PI3K/Akt signaling. We will argue that inhibitors of PI3K/Akt signaling can be components for potentially promising new CTs in both tumor entities, but further understanding of the signal cascade's complexity is essential for successful implementation of these CTs. Importantly, failure to do this might lead to severe adverse effects, such as treatment failure and enhanced therapy resistance. </p>","PeriodicalId":90271,"journal":{"name":"Molecular and cellular therapies","volume":"2 ","pages":"32"},"PeriodicalIF":0.0000,"publicationDate":"2014-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452069/pdf/","citationCount":"0","resultStr":"{\"title\":\"A critical evaluation of PI3K inhibition in Glioblastoma and Neuroblastoma therapy.\",\"authors\":\"Mike-Andrew Westhoff, Georg Karpel-Massler, Oliver Brühl, Stefanie Enzenmüller, Katia La Ferla-Brühl, Markus D Siegelin, Lisa Nonnenmacher, Klaus-Michael Debatin\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Members of the PI3K/Akt/mTor signaling cascade are among the most frequently altered proteins in cancer, yet the therapeutic application of pharmacological inhibitors of this signaling network, either as monotherapy or in combination therapy (CT) has so far not been particularly successful. In this review we will focus on the role of PI3K/Akt/mTOR in two distinct tumors, Glioblastoma multiforme (GBM), an adult brain tumor which frequently exhibits PTEN inactivation, and Neuroblastoma (NB), a childhood malignancy that affects the central nervous system and does not harbor any classic alterations in PI3K/Akt signaling. We will argue that inhibitors of PI3K/Akt signaling can be components for potentially promising new CTs in both tumor entities, but further understanding of the signal cascade's complexity is essential for successful implementation of these CTs. Importantly, failure to do this might lead to severe adverse effects, such as treatment failure and enhanced therapy resistance. </p>\",\"PeriodicalId\":90271,\"journal\":{\"name\":\"Molecular and cellular therapies\",\"volume\":\"2 \",\"pages\":\"32\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-10-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452069/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular and cellular therapies\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2014/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and cellular therapies","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2014/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

PI3K/Akt/mTor信号级联的成员是癌症中最常见的改变蛋白之一,然而该信号网络的药物抑制剂的治疗应用,无论是单一治疗还是联合治疗(CT),迄今为止都不是特别成功。在这篇综述中,我们将重点关注PI3K/Akt/mTOR在两种不同肿瘤中的作用:多形性胶质母细胞瘤(GBM),一种经常表现为PTEN失活的成人脑肿瘤,以及神经母细胞瘤(NB),一种影响中枢神经系统的儿童恶性肿瘤,PI3K/Akt信号没有任何典型的改变。我们将论证PI3K/Akt信号的抑制剂可能是这两种肿瘤实体中潜在的有前途的新ct的组成部分,但进一步了解信号级联的复杂性对于成功实施这些ct至关重要。重要的是,如果不这样做,可能会导致严重的不良反应,如治疗失败和治疗耐药性增强。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

A critical evaluation of PI3K inhibition in Glioblastoma and Neuroblastoma therapy.

A critical evaluation of PI3K inhibition in Glioblastoma and Neuroblastoma therapy.

A critical evaluation of PI3K inhibition in Glioblastoma and Neuroblastoma therapy.

A critical evaluation of PI3K inhibition in Glioblastoma and Neuroblastoma therapy.

Members of the PI3K/Akt/mTor signaling cascade are among the most frequently altered proteins in cancer, yet the therapeutic application of pharmacological inhibitors of this signaling network, either as monotherapy or in combination therapy (CT) has so far not been particularly successful. In this review we will focus on the role of PI3K/Akt/mTOR in two distinct tumors, Glioblastoma multiforme (GBM), an adult brain tumor which frequently exhibits PTEN inactivation, and Neuroblastoma (NB), a childhood malignancy that affects the central nervous system and does not harbor any classic alterations in PI3K/Akt signaling. We will argue that inhibitors of PI3K/Akt signaling can be components for potentially promising new CTs in both tumor entities, but further understanding of the signal cascade's complexity is essential for successful implementation of these CTs. Importantly, failure to do this might lead to severe adverse effects, such as treatment failure and enhanced therapy resistance.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信