J
Jason W. H. Wong
Researcher at Li Ka Shing Faculty of Medicine, University of Hong Kong
Publications - 189
Citations - 8329
Jason W. H. Wong is an academic researcher from Li Ka Shing Faculty of Medicine, University of Hong Kong. The author has contributed to research in topics: Gene & Cancer. The author has an hindex of 46, co-authored 175 publications receiving 7382 citations. Previous affiliations of Jason W. H. Wong include University of New South Wales & University College Dublin.
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Journal ArticleDOI
The Histone Methyltransferase DOT1L Promotes Neuroblastoma by Regulating Gene Transcription.
Matthew Wong,Andrew E. Tee,Giorgio Milazzo,Jessica L. Bell,Rebecca C. Poulos,Bernard Atmadibrata,Yuting Sun,Duohui Jing,Nicholas Ho,Dora Ling,Pei Yan Liu,Xudong Zhang,Stefan Hüttelmaier,Jason W. H. Wong,Jenny Y. Wang,Patsie Polly,Giovanni Perini,Christopher J. Scarlett,Tao Liu +18 more
TL;DR: DOT1L is identified as a novel cofactor in N-Myc-mediated transcriptional activation of target genes and neuroblastoma oncogenesis, and DOT1L inhibitors are characterized as novel anticancer agents against MYCN-amplified Neuroblastoma cells.
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Hydroxyl radical probe of the calmodulin-melittin complex interface by electrospray ionization mass spectrometry.
TL;DR: The N-terminus (through residue 36) of calmodulin is shown to lie in closer proximity to the melittin helix than its C-terminal counterpart (residues 127–148) based upon the protection levels measured at reactive residues within these segments of the protein.
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Noninvasive imaging of cell death using an Hsp90 ligand.
Danielle Park,Anthony S. Don,Tania Massamiri,Amol Karwa,Beth Warner,Jan MacDonald,Christine L. Hemenway,Arati D. Naik,Kah Tiong Kuan,Pierre J. Dilda,Jason W. H. Wong,Kevin Camphausen,Lori K. Chinen,Mary Dyszlewski,Philip J. Hogg +14 more
TL;DR: A small organoarsenical compound, 4-(N-(S-glutathionylacetylamino)phenylarsonous acid, that rapidly accumulates in the cytosol of dying cells coincident with loss of plasma membrane integrity, should enable the imaging of cell death in most experimental settings.
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Functional Mutations Form at CTCF-Cohesin Binding Sites in Melanoma Due to Uneven Nucleotide Excision Repair across the Motif
Rebecca C. Poulos,Julie A. I. Thoms,Yi Fang Guan,Ashwin Unnikrishnan,John E. Pimanda,Jason W. H. Wong +5 more
TL;DR: It is reported that skin cancers exhibit a highly specific asymmetric mutation pattern within CTCF motifs attributable to ultraviolet irradiation and differential nucleotide excision repair (NER), suggesting a role for cohesin in stabilizing C TCF-DNA binding and impairing NER.
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JMJD6 is a tumorigenic factor and therapeutic target in neuroblastoma.
Matthew S. Wong,Yuting Sun,Zhichao Xi,Zhichao Xi,Giorgio Milazzo,Rebecca C. Poulos,Rebecca C. Poulos,Christoph Bartenhagen,Jessica L. Bell,Chelsea Mayoh,Nicholas Ho,Andrew E. Tee,Xiaoqiong Chen,Yang Li,Roberto Ciaccio,Pei Y. Liu,Chen C. Jiang,Qing Lan,Nisitha Jayatilleke,Belamy B. Cheung,Michelle Haber,Murray D. Norris,Xu D. Zhang,Glenn M. Marshall,Jenny Y. Wang,Stefan Hüttelmaier,Matthias Fischer,Jason W. H. Wong,Jason W. H. Wong,Hong-Xi Xu,Giovanni Perini,Qihan Dong,Qihan Dong,Rani E. George,Tao Liu +34 more
TL;DR: JMJD6 is identified as a neuroblastoma tumorigenesis factor, and the combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N- myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastomas tumor regression in mice, which are significantly reversed by forced JM JD6 over-expression.