Metabolic Vulnerabilities in Brain Cancer

被引：4
|
作者：
Morrow, Danielle [1 ,3 ]
Minami, Jenna [1 ,3 ]
Nathanson, David A. [1 ,2 ,3 ]
机构：
[1] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA 90024 USA
[2] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA
[3] UCLA CHS 23-234,650 Charles E Young Dr South, Los Angeles, CA 90036 USA
来源：
NEUROSURGERY CLINICS OF NORTH AMERICA | 2021年 / 32卷 / 02期
基金：
美国国家卫生研究院;
关键词：
Metabolism; GBM; Tumor microenvironment; Oncogene; CHOLESTEROL-METABOLISM; CELLULAR-METABOLISM; HUMAN GLIOBLASTOMAS; CO-DEPENDENCY; IDH-MUTANT; CELLS; TUMORS; LANDSCAPE; OXIDATION; GROWTH;
D O I：
10.1016/j.nec.2020.12.006
中图分类号：
R74 [神经病学与精神病学];
学科分类号：
摘要：
Glioblastomas (GBMs) exhibit altered metabolism to support a variety of bioenergetic and biosynthetic demands for tumor growth, invasion, and drug resistance. Changes in glycolytic flux, oxidative phosphorylation, the pentose phosphate pathway, fatty acid biosynthesis and oxidation, and nucleic acid biosynthesis are observed in GBMs to help drive tumorigenesis. Both the genetic landscape of GBMs and the unique brain tumor microenvironment shape metabolism; therefore, an understanding of how both intrinsic and extrinsic factors modulate metabolism is becoming increasingly important for finding effect targets and therapeutics for GBM. © 2021 Elsevier Inc.
引用
收藏
页码：159 / 169
页数：11
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