Po Inglis
Royal Brisbane and Women's Hospital
10 Papers
55 Citations
Po Inglis is an academic researcher from Royal Brisbane and Women's Hospital. The author has contributed to research in topics: Glioma & Medicine. The author has an hindex of 5, co-authored 8 publications. Previous affiliations of Po Inglis include QIMR Berghofer Medical Research Institute.
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Papers
EphA3 Maintains Tumorigenicity and Is a Therapeutic Target in Glioblastoma Multiforme
Bryan W. Day,Brett W. Stringer,Fares Al-Ejeh,Michael J. Ting,John W Wilson,Kathleen S. Ensbey,Paul R. Jamieson,Zara C. Bruce,Yi Chieh Lim,Carolin Offenhäuser,Sara Charmsaz,Leanne Cooper,Jennifer K Ellacott,Angus Harding,Lucie Leveque,Po Inglis,Po Inglis,Suzanne Allan,Suzanne Allan,David G. Walker,Martin Lackmann,Geoffrey W. Osborne,Kum Kum Khanna,Brent A. Reynolds,Jason D. Lickliter,Jason D. Lickliter,Andrew W. Boyd,Andrew W. Boyd +27 more
TL;DR: Results identify EphA3 as a functional, targetable receptor in GBM and appears critically involved in maintaining tumor cells in a less differentiated state by modulating mitogen-activated protein kinase signaling.
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A reference collection of patient-derived cell line and xenograft models of proneural, classical and mesenchymal glioblastoma.
Brett W. Stringer,Bryan W. Day,Rochelle C.J. D’Souza,Paul R. Jamieson,Kathleen S. Ensbey,Zara C. Bruce,Yi Chieh Lim,Kate Goasdoué,Carolin Offenhäuser,Seckin Akgul,Suzanne Allan,Suzanne Allan,Thomas Robertson,Peter Lucas,Gert Tollesson,S. Campbell,Craig Winter,Hongdo Do,Alexander Dobrovic,Po Inglis,Po Inglis,Rosalind L. Jeffree,Rosalind L. Jeffree,Terrance Grant Johns,Andrew W. Boyd,Andrew W. Boyd +25 more
TL;DR: A curated panel of 12 readily-usable, genetically-diverse, tumourigenic, patient-derived, low-passage, serum-free cell lines representing the spectrum of molecular subtypes of IDH-wildtype GBM along with their detailed phenotypic characterisation plus a bespoke set of lentiviral plasmids for bioluminescent/fluorescent labelling, gene expression and CRISPR/Cas9-mediated gene inactivation are presented.
ELK4 neutralization sensitizes glioblastoma to apoptosis through downregulation of the anti-apoptotic protein Mcl-1.
Bryan W. Day,Brett W. Stringer,Mark D. Spanevello,Mark D. Spanevello,Sara Charmsaz,Paul R. Jamieson,Kathleen S. Ensbey,Jacinta C. Carter,Joanne M. Cox,Vicky J. Ellis,Christopher L. Brown,David G. Walker,Po Inglis,Suzanne Allan,Suzanne Allan,Brent A. Reynolds,Jason D. Lickliter,Andrew W. Boyd,Andrew W. Boyd +18 more
TL;DR: The ETS transcription factor ELK4 was identified as a critical regulator of Mcl-1 in glioma, since ELK3 downregulation was shown to reduce M cl-1 and increase sensitivity to apoptosis, and in vivo, ELK 4 downregulation reduced tumor formation inglioblastoma xenograft models.
The dystroglycan receptor maintains glioma stem cells in the vascular niche.
Bryan W. Day,Bryan W. Day,Bryan W. Day,Justin D. Lathia,Zara C. Bruce,Rochelle C.J. D’Souza,Ulrich Baumgartner,Kathleen S. Ensbey,Yi Chieh Lim,Brett W. Stringer,Seckin Akgul,Carolin Offenhäuser,Yuchen Li,Paul R. Jamieson,Fiona M. Smith,Courtney L.R. Jurd,Thomas Robertson,Po Inglis,Zarnie Lwin,Rosalind L. Jeffree,Terrance Grant Johns,Krishna P.L. Bhat,Jeremy N. Rich,Kevin P. Campbell,Andrew W. Boyd,Andrew W. Boyd +25 more
TL;DR: A central role of the DG receptor is revealed, not only as a structural element, but also as a critical factor promoting MES-like GBM and the maintenance of GSCs residing in the perivascular niche.
Preliminary findings of a phase i safety and bioimaging trial of kb004 (ifabotuzumab) in patients with glioblastoma
Hui K Gan,Lawrence Cher,Po Inglis,Zarnie Lwin,Eddie Lau,Uwe Ackermann,Nicole Coombs,Kirsten Remen,Nancy Guo,Sze Ting Lee,Sylvia J. Gong,Jodie Palmer,Kunthi Pathmaraj,Graeme O'Keefe,Fiona Scott,Bryan W. Day,Andrew W. Boyd,Paul Thomas,Cameron Durrant,Andrew M. Scott +19 more
TL;DR: 89Zr-ifab PET/CT scans showed rapid, specific targeting at all known tumor sites and in all pts, but no normal tissue uptake, which was consistent with treatment effect on tumor vasculature, and MRI scans showed predominant T2/FLAIR changes, occasionally marked.