Gliomas are tumors that originate from glial cells in the central nervous system (the brain and spinal cord),      accounting for approximately 40%-50% of all primary brain tumors. They are also one of the most common and      malignant types of tumors in adults' central nervous system. Based on the originating cell type, they can be      classified into astrocytomas, ependymomas, or oligodendrogliomas. Due to their infiltrative growth characteristics,      they are difficult to treat, have a high recurrence rate, and significantly impact the neurological function and      survival period of patients^[1,2].

     At the molecular level, the occurrence of gliomas is closely related to various genetic mutations and abnormalities      in signaling pathways. For example, IDH mutations, inactivation of TP53 and RB1 genes, mutations in genes such as      EGFR and PDGFRA, and abnormal activation of RAS/MAPK and PI3K/AKT/mTOR signaling pathways all contribute to the      development and progression of gliomas. Additionally, epigenetic modifications, such as abnormal DNA methylation      and histone modifications, also regulate gene expression and influence tumor progression^[3].

     The pathogenesis of gliomas also involves the tumor microenvironment and immune escape. Glioma cells achieve immune      escape by inhibiting T cell function, promoting the activation and differentiation of immunosuppressive cells      (such as macrophages and dendritic cells), and upregulating the expression of immune checkpoint molecules.      Furthermore, abnormal metabolic pathways in gliomas, such as fatty acid metabolism and purine metabolism, may also      become new targets for treatment^[4].

     The pathogenesis of gliomas is complex, involving various molecular, genetic, and environmental factors. In-depth      research into the molecular mechanisms of these signaling pathways will help develop more effective diagnostic and      therapeutic strategies.

The molecular mechanisms of metabolism, signal transduction, and interaction with tumor-associated blood vessels in glioma cells^[5].

Target Proteins Associated with Glioma ：

ELISA Kits：

References：

1.        Yei J, Lee NK, Ryu S, Ryu SE, Lee J, Park T, Jeong Y, Kang R, Kwon HK, Kim SG, Park JC, Park CG, Suh M. Glioma-Associated Microglia Potentiate Neuronal Hyper-Excitability in the Glioma Environment. Neuro Oncol. 2025 Jul 30:noaf181. Epub ahead of print. PMID: 40741716.
2.        Poorva P, Mast J, Cao B, Shah MV, Pollok KE, Shen J. Killing the killers: Natural killer cell therapy targeting glioma stem cells in high-grade glioma. Mol Ther. 2025 Jun 4;33(6):2462-2478. Epub 2025 Mar 3. PMID: 40040281.
3.        He Y, Li W, Zhang X, Cui Z. Oncolytic Virus Targeted Therapy for Glioma via Intravenous Delivery. Adv Healthc Mater. 2025 Mar;14(7):e2404965. Epub 2025 Jan 13. PMID: 39801205.
4.        Luo K, Zhuang K, Wu H, Chen Y, Liu Y, Yang F, Wang Z. PLIN1 suppresses glioma progression through regulating lipid metabolism. Cell Death Dis. 2025 Jan 27;16(1):48. PMID: 39870645.

Flora Flora is a technical support expert at EnkiLife, familiar with immunology and neuroscience, dedicated to providing customers with high-quality product combinations and technical support to help achieve research in neurodegenerative diseases and other neuroscience areas.