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肿瘤代谢:治疗神经胶质瘤的新领域。

Tumor Metabolism: A New Field for the Treatment of Glioma.

机构信息

School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.

Jiangsu Provincial TCM Engineering Technology Research Center of High Efficient Drug Delivery System, Nanjing 210023, China.

出版信息

Bioconjug Chem. 2024 Aug 21;35(8):1116-1141. doi: 10.1021/acs.bioconjchem.4c00287. Epub 2024 Jul 16.

DOI:10.1021/acs.bioconjchem.4c00287
PMID:39013195
Abstract

The clinical treatment of glioma remains relatively immature. Commonly used clinical treatments for gliomas are surgery combined with chemotherapy and radiotherapy, but there is a problem of drug resistance. In addition, immunotherapy and targeted therapies also suffer from the problem of immune evasion. The advent of metabolic therapy holds immense potential for advancing more efficacious and tolerable therapies against this aggressive disease. Metabolic therapy alters the metabolic processes of tumor cells at the molecular level to inhibit tumor growth and spread, and lead to better outcomes for patients with glioma that are insensitive to conventional treatments. Moreover, compared with conventional therapy, it has less impact on normal cells, less toxicity and side effects, and higher safety. The objective of this review is to examine the changes in metabolic characteristics throughout the development of glioma, enumerate the current methodologies employed for studying tumor metabolism, and highlight the metabolic reprogramming pathways of glioma along with their potential molecular mechanisms. Importantly, it seeks to elucidate potential metabolic targets for glioblastoma (GBM) therapy and summarize effective combination treatment strategies based on various studies.

摘要

脑胶质瘤的临床治疗仍相对不成熟。脑胶质瘤常用的临床治疗方法是手术联合化疗和放疗,但存在耐药问题。此外,免疫疗法和靶向疗法也存在免疫逃逸问题。代谢疗法的出现为开发针对这种侵袭性疾病更有效和更耐受的治疗方法提供了巨大的潜力。代谢疗法在分子水平上改变肿瘤细胞的代谢过程,抑制肿瘤生长和扩散,为对常规治疗不敏感的脑胶质瘤患者带来更好的结果。此外,与传统疗法相比,它对正常细胞的影响较小,毒性和副作用较小,安全性更高。本综述的目的是研究脑胶质瘤发展过程中代谢特征的变化,列举目前用于研究肿瘤代谢的方法,并强调脑胶质瘤的代谢重编程途径及其潜在的分子机制。重要的是,它旨在阐明胶质母细胞瘤(GBM)治疗的潜在代谢靶点,并根据各种研究总结有效的联合治疗策略。

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Cysteine‑ and glycine‑rich protein 2: A vital regulator that inhibits necroptosis glioma cell by activating the JAK‑STAT1 pathways.
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