血管内皮生长因子、血管内皮生长因子受体、磷酸化信号转导因子及转录因子3在恶性胶质瘤中的表达与关联

IF 0.8 Q4 CLINICAL NEUROLOGY Journal of Neurosciences in Rural Practice Pub Date : 2023-09-18 DOI:10.25259/jnrp_155_2023
Praveena Edura, Ramya Vokuda, Subhashini Ramamoorthi, Bheemanathi Hanuman Srinivas, Surendar Kumar Verma, Gopalakrishnan Sasidharan
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引用次数: 0

摘要

目的:血管生成是恶性胶质瘤的主要特征之一。磷酸化信号转导因子3 (pSTAT3)不仅参与胶质瘤细胞的增殖、抗凋亡和免疫抑制,而且在细胞迁移和侵袭中起关键作用。组成性地,激活的pSTAT3诱导血管内皮生长因子(VEGF)及其受体VEGFR的表达,导致内皮细胞增殖和异常微血管形成,导致肿瘤周围水肿(PTE)。PTE是恶性胶质瘤死亡的重要原因之一。因此,了解胶质瘤进化的分子机制是必要的。本研究旨在评估恶性胶质瘤中pSTAT3、VEGF和VEGFR的表达水平,并分析PTE的程度以及其中一种或多种标志物的表达程度。材料与方法:本研究纳入84例按照世界卫生组织中枢神经系统肿瘤分类分为IV级、III级和II级胶质瘤的患者,通过免疫组化研究pSTAT3、VEGF和VEGFR的表达。此外,使用磁共振成像/计算机断层扫描来确定这些患者是否存在PTE。结果:pSTAT3、VEGFR、VEGF标志物与PTE程度的相关性有统计学意义(P <0.05)。结论:pSTAT3、VEGF- r和VEGF信号通路参与了肿瘤发生和发展过程中PTE形成的调控机制。
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Expression and association of vascular endothelial growth factor, vascular endothelial growth factor receptor, and phosphorylated signal transducer and activator of transcription factor 3 in malignant gliomas
Objectives: Angiogenesis is one of the main characteristic features of malignant gliomas. Phosphorylated signal transducer and activator of transcription factor 3 (pSTAT3) is not only involved in glioma cell proliferation, anti-apoptosis, and immunosuppression but also plays a key role in cell migration and invasion. Constitutively, activated pSTAT3 induces expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR, leading to endothelial cell proliferation and abnormal microvascular formation causing peritumoral edema (PTE). PTE is one of the significant contributors to mortality in malignant gliomas. Therefore, understanding the molecular mechanism involved in the evolution of gliomas is necessary. This study was to assess the level of expression of pSTAT3, VEGF, and VEGFR in malignant gliomas and analyze the extent of PTE and the extent of expression of one or more of these markers. Materials and Methods: This study included 84 patients categorized as per the World Health Organization classification of central nervous system tumors into grade IV, III, and II gliomas to investigate the expression of pSTAT3, VEGF, and VEGFR by immunohistochemistry. Furthermore, the presence or absence of PTE was determined using magnetic resonance imaging/computed tomography scans in these patients. Results: The association between the markers (pSTAT3, VEGFR, and VEGF) and the extent of PTE in these patients was statistically significant ( P < 0.05). Conclusion: The pSTAT3, VEGF-R, and VEGF signaling pathways could contribute to peritumoral edema and might be a regulatory mechanism during PTE formation during tumorigenesis and progression.
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129
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22 weeks
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