PDF(Pubmed)
Abstract：
Gliomas\' aggressive nature and resistance to therapy make them a major problem in oncology. Gliomas continue to have dismal prognoses despite significant advancements in medical science, and traditional treatments like surgery, radiation (RT), and chemotherapy (CT) frequently prove to be ineffective. After glioma stem cells (GSCs) were discovered, the traditional view of gliomas as homogeneous masses changed. GSCs are essential for tumor growth, treatment resistance, and recurrence. These cells\' distinct capacities for differentiation and self-renewal are changing our knowledge of the biology of gliomas. This systematic literature review aims to uncover the molecular mechanisms driving glioma progression associated with GSCs. The systematic review adhered to PRISMA guidelines, with a thorough literature search conducted on PubMed, Ovid MED-LINE, and Ovid EMBASE. The first literature search was performed on 1 March 2024, and the search was updated on 15 May 2024. Employing MeSH terms and Boolean operators, the search focused on molecular mechanisms associated with GCSs-mediated glioma progression. Inclusion criteria encompassed English language studies, preclinical studies, and clinical trials. A number of 957 papers were initially identified, of which 65 studies spanning from 2005 to 2024 were finally included in the review. The main GSC model distribution is arranged in decreasing order of frequency: U87: 20 studies (32.0%); U251: 13 studies (20.0%); A172: 4 studies (6.2%); and T98G: 2 studies (3.17%). From most to least frequent, the distribution of the primary GSC pathway is as follows: Notch: 8 studies (12.3%); STAT3: 6 studies (9.2%); Wnt/β-catenin: 6 studies (9.2%); HIF: 5 studies (7.7%); and PI3K/AKT: 4 studies (6.2%). The distribution of molecular effects, from most to least common, is as follows: inhibition of differentiation: 22 studies (33.8%); increased proliferation: 18 studies (27.7%); enhanced invasive ability: 15 studies (23.1%); increased self-renewal: 5 studies (7.7%); and inhibition of apoptosis: 3 studies (4.6%). This work highlights GSC heterogeneity and the dynamic interplay within the glioblastoma microenvironment, underscoring the need for a tailored approach. A few key pathways influencing GSC behavior are JAK/STAT3, PI3K/AKT, Wnt/β-catenin, and Notch. Therapy may target these pathways. This research urges more study to fill in knowledge gaps in the biology of GSCs and translate findings into useful treatment approaches that could improve GBM patient outcomes.
摘要：
胶质瘤的侵袭性和对治疗的抵抗力使其成为肿瘤学的主要问题。尽管医学科学取得了重大进展，但胶质瘤的预后仍然令人沮丧，和传统的治疗方法，如手术，辐射(RT),和化疗（CT）经常被证明是无效的。神经胶质瘤干细胞（GSCs）被发现后，将胶质瘤视为均匀肿块的传统观点发生了变化。GSC对肿瘤生长至关重要，治疗抗性，和复发。这些细胞不同的分化和自我更新能力正在改变我们对胶质瘤生物学的认识。本系统文献综述旨在揭示与GSCs相关的神经胶质瘤进展的分子机制。系统审查遵循PRISMA准则，在PubMed上进行了彻底的文献检索，Ovid医疗系统,OvidEmbase.首次文献检索于2024年3月1日进行，检索于2024年5月15日更新。使用MeSH术语和布尔运算符，本研究的重点是与GCSs介导的神经胶质瘤进展相关的分子机制.纳入标准包括英语语言研究，临床前研究,和临床试验。最初确定了957篇论文，其中2005年至2024年的65项研究最终被纳入综述。主要GSC模型分布按频率降序排列:U87:20项研究(32.0%);U251:13项研究(20.0%);A172:4项研究(6.2%);T98G:2项研究(3.17%)。从最频繁到最不频繁，主要GSC途径的分布如下:Notch:8项研究(12.3%);STAT3:6项研究(9.2%);Wnt/β-catenin:6项研究(9.2%);HIF:5项研究(7.7%);PI3K/AKT:4项研究(6.2%)。分子效应的分布，从最常见到最不常见，如下:分化抑制:22项研究(33.8%);增殖增加:18项研究(27.7%);侵袭能力增强:15项研究(23.1%);自我更新增加:5项研究(7.7%);凋亡抑制:3项研究(4.6%)。这项工作强调了GSC异质性和胶质母细胞瘤微环境内的动态相互作用，强调需要一种量身定制的方法。影响GSC行为的一些关键途径是JAK/STAT3，PI3K/AKT，Wnt/β-catenin,还有Notch.治疗可以针对这些途径。这项研究敦促更多的研究来填补GSCs生物学方面的知识空白，并将发现转化为可以改善GBM患者预后的有用治疗方法。
