V
V. Wee Yong
Researcher at University of Calgary
Publications - 276
Citations - 21024
V. Wee Yong is an academic researcher from University of Calgary. The author has contributed to research in topics: Multiple sclerosis & Microglia. The author has an hindex of 73, co-authored 233 publications receiving 17556 citations. Previous affiliations of V. Wee Yong include Allen Institute for Brain Science & Foothills Medical Centre.
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Journal ArticleDOI
Single-cell RNA-seq reveals that glioblastoma recapitulates a normal neurodevelopmental hierarchy
Charles P. Couturier,Shamini Ayyadhury,Phuong Uyen Le,Javad Nadaf,Javad Nadaf,Jean Monlong,Gabriele Riva,Redouane Allache,Salma Baig,Xiaohua Yan,Mathieu Bourgey,Changseok Lee,Yu Chang David Wang,V. Wee Yong,Marie-Christine Guiot,Hamed S. Najafabadi,Bratislav Misic,Jack P. Antel,Guillaume Bourque,Jiannis Ragoussis,Kevin Petrecca +20 more
TL;DR: A conserved neural tri-lineage cancer hierarchy centered around glial progenitor-like cells is found, and this hierarchal map can be used to identify therapeutic targets specific to progenitors cancer stem cells.
Journal Article
Induction and intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediated apotosis in human malignant glioma cells.
Chunhai Hao,Francesco Beguinot,Gerolama Condorelli,Alessandra Trencia,Erwin G. Van Meir,V. Wee Yong,Ian F. Parney,Wilson Roa,Kenneth C. Petruk +8 more
TL;DR: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) preferentially triggers apoptosis in tumor cells versus normal cells, thus providing a therapeutic potential and may be exploitable for glioma and possibly for other cancer therapies.
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Interleukin‐1β promotes oligodendrocyte death through glutamate excitotoxicity
TL;DR: The results provide a mechanistic link between the persistent and insidious microglia activation that is evident in all stages of multiple sclerosis, with the recent appreciation that glutamate excitotoxicity leads to the destruction of oligodendrocytes in the disease.
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Progressive multiple sclerosis: from pathophysiology to therapeutic strategies.
TL;DR: The pathophysiological complexity of progressive multiple sclerosis challenges the development of effective treatments, despite the substantial unmet clinical need, and the need for therapies that target inflammation, neurodegeneration and remyelination will likely be needed in combination.
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Differential mechanisms of action of interferon-β and glatiramer acetate in MS
TL;DR: The presence of GA-reactive lymphocytes within the CNS parenchyma may have the additional benefit of conferring neuroprotection through protective autoimmunity.