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glioblastoma cells

PI3Kγ Inhibition Suppresses Microglia/TAM Accumulation in Glioblastoma Microenvironment to Promote Exceptional Temozolomide Response

[Proceedings of the National Academy of Sciences of the United States of America] Glioblastoma-associated microglia/macrophages secreted interleukin 11 activated STAT3-MYC signaling in glioblastoma cells. This signaling induced stem cell states that conferred enhanced tumorigenicity and resistance to the standard-of-care chemotherapy, temozolomide.

Tumor Cell Plasticity, Heterogeneity, and Resistance in Crucial Microenvironmental Niches in Glioma

[Nature Communications] Scientists identified NOTCH1 as a central switch between the perivascular niche and network niche in glioma, and demonstrated robust cross-compensation when only one niche was targeted.

SOX1 Is a Backup Gene for Brain Neurons and Glioma Stem Cell Protection and Proliferation

[Molecular Neurobiology] The authors collate the most important discoveries relating to the neuroprotective effects of SOX1 in brain cancer and propose hypothesis worthy of SOX1’s role in the survival of senescent neuronal cells, its roles in fibroblast cell proliferation, and cell fate for neuroprotection, and the discharge of electrical impulses for homeostasis.

Modulation of Nogo Receptor 1 Expression Orchestrates Myelin-Associated Infiltration of Glioblastoma

[Brain] Investigators adopted a radiogenomic analysis to screen for functionally relevant genes that orchestrated the process of glioma cell infiltration through myelin and promoted glioblastoma aggressiveness.

ADO/Hypotaurine: A Novel Metabolic Pathway Contributing to Glioblastoma Development

[Cell Death Discovery] The authors identified hypotaurine as one of the top-ranked metabolites for differentiating low- and high-grade tumors, and that there was also a strong association between the levels of intratumoral hypotaurine and expression of its biosynthetic enzyme, cysteamine (2-aminoethanethiol) dioxygenase.

Histone Demethylase KDM4C Controls Tumorigenesis of Glioblastoma by Epigenetically Regulating p53 and C-Myc

[Cell Death & Disease] Researchers showed that KDM4C knockdown significantly repressed proliferation and tumorigenesis of glioblastoma cells in vitro and in vivo that were rescued by overexpressing wild-type KDM4C but not a catalytic dead mutant.

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