Poliovirus Recombinants Against Malignant Glioma

2004 ◽  
pp. 755-796
Keyword(s):  
Malignant Glioma

Therapeutic management of malignant glioma in pregnancy: a case report highlighting clinical and radiological features at diagnosis and after intervention

2020 ◽  
Vol 3 (68) ◽  
pp. 147
Author(s):  
Ioniţă Ducu ◽  
Roxana-Elena Bohîlţea ◽  
Dan Teleanu ◽  
Natalia Ţurcan ◽  
Monica Mihaela Cîrstoiu
Keyword(s):  
Case Report ◽  
Malignant Glioma ◽  
Therapeutic Management ◽  
Radiological Features ◽  
In Pregnancy

Hypoxia and the Malignant Glioma Microenvironment: Regulation and Implications for Therapy

2009 ◽  
Vol 2 (3) ◽  
pp. 263-284 ◽  
Author(s):  
L. Oliver ◽  
C. Olivier ◽  
F. Marhuenda ◽  
M. Campone ◽  
F. Vallette
Keyword(s):  
Malignant Glioma ◽  
Glioma Microenvironment

scholarly journals Overexpression of hyaluronan-binding protein 1 promotes the proliferation, migration, and invasion of malignant glioma

2020 ◽  
Vol 9 (1) ◽  
pp. 1-11
Author(s):  
Zijun Yang ◽  
Shu Song ◽  
Wenchao Yin ◽  
Xin Qian ◽  
Qiang Yu ◽  
...  
Keyword(s):  
Malignant Glioma ◽  
Binding Protein ◽  
Migration And Invasion ◽  
Hyaluronan Binding

scholarly journals Improving vaccine efficacy against malignant glioma

2016 ◽  
Vol 5 (8) ◽  
pp. e1196311 ◽  
Author(s):  
Erik Ladomersky ◽  
Matthew Genet ◽  
Lijie Zhai ◽  
Galina Gritsina ◽  
Kristen L. Lauing ◽  
...  
Keyword(s):  
Malignant Glioma ◽  
Vaccine Efficacy

scholarly journals Sequential fate-switches in stem-like cells drive the tumorigenic trajectory from human neural stem cells to malignant glioma

Cell Research ◽  
2021 ◽  
Author(s):  
Xiaofei Wang ◽  
Ran Zhou ◽  
Yanzhen Xiong ◽  
Lingling Zhou ◽  
Xiang Yan ◽  
...  
Keyword(s):  
Malignant Glioma ◽  
Single Cell ◽  
De Novo ◽  
Early Stage ◽  
Lineage Tracing ◽  
Human Neural Stem Cells ◽  
Transcriptional Reprogramming ◽  
Neural Stem Progenitor Cells ◽  
Human Gbm ◽  
End Stage

AbstractGlioblastoma (GBM) is an incurable and highly heterogeneous brain tumor, originating from human neural stem/progenitor cells (hNSCs/hNPCs) years ahead of diagnosis. Despite extensive efforts to characterize hNSCs and end-stage GBM at bulk and single-cell levels, the de novo gliomagenic path from hNSCs is largely unknown due to technical difficulties in early-stage sampling and preclinical modeling. Here, we established two highly penetrant hNSC-derived malignant glioma models, which resemble the histopathology and transcriptional heterogeneity of human GBM. Integrating time-series analyses of whole-exome sequencing, bulk and single-cell RNA-seq, we reconstructed gliomagenic trajectories, and identified a persistent NSC-like population at all stages of tumorigenesis. Through trajectory analyses and lineage tracing, we showed that tumor progression is primarily driven by multi-step transcriptional reprogramming and fate-switches in the NSC-like cells, which sequentially generate malignant heterogeneity and induce tumor phenotype transitions. We further uncovered stage-specific oncogenic cascades, and among the candidate genes we functionally validated C1QL1 as a new glioma-promoting factor. Importantly, the neurogenic-to-gliogenic switch in NSC-like cells marks an early stage characterized by a burst of oncogenic alterations, during which transient AP-1 inhibition is sufficient to inhibit gliomagenesis. Together, our results reveal previously undercharacterized molecular dynamics and fate choices driving de novo gliomagenesis from hNSCs, and provide a blueprint for potential early-stage treatment/diagnosis for GBM.

Modulation effects of hexamethylene bisacetamide on growth and differentiation of cultured human malignant glioma cells

1996 ◽  
Vol 84 (5) ◽  
pp. 831-838 ◽  
Author(s):  
Xiao-Nan Li ◽  
Zi-Wei Du ◽  
Qiang Huang
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Malignant Glioma ◽  
Culture Media ◽  
Morphological Changes ◽  
Control Group ◽  
Cell Cycle Distribution ◽  
Content Type ◽  
Hexamethylene Bisacetamide ◽  
Human Malignant Glioma

✓ The modulation effects of hexamethylene bisacetamide (HMBA), a differentiation-inducing agent, on growth and differentiation of cells from human malignant glioma cell line SHG-44 were studied. At cytostatic doses (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 15 days), HMBA exerted a marked inhibitory effect on cell proliferation. Exposure to HMBA (5 mM and 10 mM for 12 days) also resulted in an accumulation of cells in G0/G1 phase and a decrease of cells in S phase as analyzed by flow cytometry. The reversible effects of 7.5 mM HMBA and 10 mM HMBA on cell proliferation and 10 mM HMBA on disruption of cell cycle distribution were observed when HMBA was removed from culture media on Day 6 and replaced with HMBA-free media. Colony-forming efficiency (CFE) in soft agar was remarkably decreased by HMBA (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 14 days), and in 7.5 mM HMBA— and 10 mM HMBA—treated cells, the CFEs were reduced to 25% and 12.5%, respectively, of that in untreated cells. Cells treated with HMBA (5 mM and 10 mM for 15 days) remained tumorigenic in athymic nude mice, but the growth rates of the xenografts were much slower than those in the control group. The effects of HMBA on cell proliferation, cell cycle distribution, CFE, and growth of xenografts were dose dependent. A more mature phenotype was confirmed by the morphological changes from spindle shape to large polygonal stellate shape and remarkably elevated expression of glial fibrillary acidic protein in cells exposed to HMBA (5 mM, 10 mM for 15 days). Our results showed that a more differentiated phenotype with marked growth arrest was induced in SHG-44 cells by HMBA.

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