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本文引用的文献

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The Intratumoral Heterogeneity of Cancer Metabolism.肿瘤内代谢异质性。
Adv Exp Med Biol. 2021;1311:149-160. doi: 10.1007/978-3-030-65768-0_11.
2
Different Tumor Microenvironments Lead to Different Metabolic Phenotypes.不同的肿瘤微环境导致不同的代谢表型。
Adv Exp Med Biol. 2021;1311:137-147. doi: 10.1007/978-3-030-65768-0_10.
3
The Heterogeneity of Lipid Metabolism in Cancer.癌症中的脂质代谢异质性。
Adv Exp Med Biol. 2021;1311:39-56. doi: 10.1007/978-3-030-65768-0_3.
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Glutamine Metabolism in Cancer.癌症中的谷氨酰胺代谢
Adv Exp Med Biol. 2021;1311:17-38. doi: 10.1007/978-3-030-65768-0_2.
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Glucose Metabolism in Cancer: The Warburg Effect and Beyond.癌症中的葡萄糖代谢:瓦伯格效应及其他
Adv Exp Med Biol. 2021;1311:3-15. doi: 10.1007/978-3-030-65768-0_1.
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Metabolic heterogeneity and adaptability in brain tumors.脑肿瘤中的代谢异质性和适应性。
Cell Mol Life Sci. 2020 Dec;77(24):5101-5119. doi: 10.1007/s00018-020-03569-w. Epub 2020 Jun 6.
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Advances in the Knowledge of the Molecular Biology of Glioblastoma and Its Impact in Patient Diagnosis, Stratification, and Treatment.胶质母细胞瘤分子生物学知识的进展及其对患者诊断、分层和治疗的影响。
Adv Sci (Weinh). 2020 Mar 12;7(9):1902971. doi: 10.1002/advs.201902971. eCollection 2020 May.
8
Cerebrospinal fluid tumor DNA for liquid biopsy in glioma patients' management: Close to the clinic?脑脊髓液肿瘤 DNA 进行液体活检在胶质瘤患者管理中的应用:接近临床?
Crit Rev Oncol Hematol. 2020 Feb;146:102879. doi: 10.1016/j.critrevonc.2020.102879. Epub 2020 Jan 24.
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Application of metabolomics technologies toward cancer prognosis and therapy.代谢组学技术在癌症预后和治疗中的应用。
Int Rev Cell Mol Biol. 2019;347:191-223. doi: 10.1016/bs.ircmb.2019.07.003. Epub 2019 Aug 7.
10
Uncovering the Role of N-Acetyl-Aspartyl-Glutamate as a Glutamate Reservoir in Cancer.揭示 N-乙酰天冬氨酸谷氨酸作为癌症中谷氨酸储备库的作用。
Cell Rep. 2019 Apr 9;27(2):491-501.e6. doi: 10.1016/j.celrep.2019.03.036.

多面性胶质母细胞瘤:从基因组改变到代谢适应。

The Multifaceted Glioblastoma: From Genomic Alterations to Metabolic Adaptations.

机构信息

Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Department of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Adv Exp Med Biol. 2021;1311:59-76. doi: 10.1007/978-3-030-65768-0_4.

DOI:10.1007/978-3-030-65768-0_4
PMID:34014534
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9703277/
Abstract

Glioblastoma multiforme (GBM) develops on glial cells and is the most common as well as the deadliest form of brain cancer. As in other cancers, distinct combinations of genetic alterations in GBM subtypes induce a diversity of metabolic phenotypes, which explains the variability of GBM sensitivity to current therapies targeting its reprogrammed metabolism. Therefore, it is becoming imperative for cancer researchers to account for the temporal and spatial heterogeneity within this cancer type before making generalized conclusions about a particular treatment's efficacy. Standard therapies for GBM have shown little success as the disease is almost always lethal; however, researchers are making progress and learning how to combine therapeutic strategies most effectively. GBMs can be classified initially into two subsets consisting of primary and secondary GBMs, and this categorization stems from cancer development. GBM is the highest grade of gliomas, which includes glioma I (low proliferative potential), glioma II (low proliferative potential with some capacity for infiltration and recurrence), glioma III (evidence of malignancy), and glioma IV (GBM) (malignant with features of necrosis and microvascular proliferation). Secondary GBM develops from a low-grade glioma to an advanced-stage cancer, while primary GBM provides no signs of progression and is identified as an advanced-stage glioma from the onset. The differences in prognosis and histology correlated with each classification are generally negligible, but the demographics of individuals affected and the accompanying genetic/metabolic properties show distinct differentiation [3].

摘要

多形性胶质母细胞瘤(GBM)起源于神经胶质细胞,是最常见也是最致命的脑癌类型。与其他癌症一样,GBM 亚型中不同的基因突变组合会诱导出多种代谢表型,这也解释了 GBM 对当前针对其重编程代谢的治疗方法的敏感性存在差异。因此,癌症研究人员在对特定治疗方法的疗效做出一般性结论之前,必须考虑到这种癌症类型的时间和空间异质性。由于这种疾病几乎总是致命的,因此 GBM 的标准治疗方法收效甚微;然而,研究人员正在取得进展,并学习如何最有效地结合治疗策略。GBM 最初可以分为两个子集,包括原发性和继发性 GBM,这种分类源于癌症的发展。GBM 是神经胶质瘤的最高级别,包括神经胶质瘤 I(低增殖潜能)、神经胶质瘤 II(低增殖潜能,具有一定的浸润和复发能力)、神经胶质瘤 III(恶性证据)和神经胶质瘤 IV(GBM)(恶性,具有坏死和微血管增殖特征)。继发性 GBM 由低级别胶质瘤发展为晚期癌症,而原发性 GBM 没有进展的迹象,从一开始就被确定为晚期胶质瘤。与每种分类相关的预后和组织学差异通常可以忽略不计,但受影响个体的人口统计学特征和伴随的遗传/代谢特征显示出明显的分化[3]。