'Slicing' glioblastoma drivers with the Swiss cheese model

被引：3

作者：

Pumar, Oriana Y. Teran ^{[1
,2
]}

Lathia, Justin D. ^{[3
,4
]}

Watson, Dionysios C. ^{[1
,5
]}

Bayik, Defne ^{[1
,2
]}

机构：

[1] Univ Miami, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA

[2] Univ Miami, Miller Sch Med, Dept Mol & Cellular Pharmacol, Miami, FL 33136 USA

[3] Case Comprehens Canc Ctr, Cleveland, OH 44195 USA

[4] Lerner Res Inst, Cleveland, OH USA

[5] Univ Miami, Miller Sch Med, Med Oncol Div, Miami, FL 33136 USA

来源：

TRENDS IN CANCER | 2024年 / 10卷 / 01期

基金：

美国国家卫生研究院;

关键词：

CANCER STEM-CELLS; SURVIVAL; HYPOXIA; MUTATIONS; STAT3; PROLIFERATION; TEMOZOLOMIDE; INHIBITOR; SUBTYPES; REVEALS;

D O I：

10.1016/j.trecan.2023.08.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The Swiss cheese model is used to assess risks and explain accidents in a variety of industries. This model can be applied to dissect the homeostatic mechanisms whose cumulative dysregulation contributes to disease states, including cancer. Using glioblastoma (GBM) as an exemplar, we discuss how specific protumorigenic mechanisms collectively drive disease by affecting genomic integrity, epigenetic regulation, metabolic homeostasis, and antitumor immunity. We further highlight how host factors, such as hormonal differences and aging, impact this process, and the interplay between these 'system failures' that enable tumor progression and foster therapeutic resistance. Finally, we examine therapies that consider the interactions between these elements, which may comprise more effective approaches given the multifaceted protumorigenic mechanisms that drive GBM.

引用

页码：15 / 27

页数：13

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