Author
Listed:
- Branavan Manoranjan
(University of Calgary
McMaster University
McMaster University)
- Chitra Venugopal
(McMaster University
McMaster University)
- David Bakhshinyan
(McMaster University
McMaster University)
- Ashley A. Adile
(McMaster University
McMaster University)
- Laura Richards
(University Health Network
University of Toronto)
- Michelle M. Kameda-Smith
(McMaster University
McMaster University)
- Owen Whitley
(University of Toronto
University of Toronto)
- Anna Dvorkin-Gheva
(McMaster University)
- Minomi Subapanditha
(McMaster University)
- Neil Savage
(McMaster University)
- Nazanin Tatari
(McMaster University)
- Dillon McKenna
(McMaster University
McMaster University)
- Blessing Bassey-Archibong
(McMaster University)
- Neil Winegarden
(University Health Network
University of Toronto)
- Robin Hallett
(Northern Biologics)
- John P. Provias
(McMaster University)
- Blake Yarascavitch
(McMaster University)
- Olufemi Ajani
(McMaster University)
- Adam Fleming
(McMaster University)
- Gary D. Bader
(University of Toronto
University of Toronto
University of Toronto)
- Trevor J. Pugh
(University Health Network
University of Toronto)
- Bradley W. Doble
(McMaster University
McMaster University
University of Manitoba
University of Manitoba)
- Sheila K. Singh
(McMaster University
McMaster University
McMaster University)
Abstract
Medulloblastoma (MB) is defined by four molecular subgroups (Wnt, Shh, Group 3, Group 4) with Wnt MB having the most favorable prognosis. Since prior reports have illustrated the antitumorigenic role of Wnt activation in Shh MB, we aimed to assess the effects of activated canonical Wnt signaling in Group 3 and 4 MBs. By using primary patient-derived MB brain tumor-initiating cell (BTIC) lines, we characterize differences in the tumor-initiating capacity of Wnt, Group 3, and Group 4 MB. With single cell RNA-seq technology, we demonstrate the presence of rare Wnt-active cells in non-Wnt MBs, which functionally retain the impaired tumorigenic potential of Wnt MB. In treating MB xenografts with a Wnt agonist, we provide a rational therapeutic option in which the protective effects of Wnt-driven MBs may be augmented in Group 3 and 4 MB and thereby support emerging data for a context-dependent tumor suppressive role for Wnt/β-catenin signaling.
Suggested Citation
Branavan Manoranjan & Chitra Venugopal & David Bakhshinyan & Ashley A. Adile & Laura Richards & Michelle M. Kameda-Smith & Owen Whitley & Anna Dvorkin-Gheva & Minomi Subapanditha & Neil Savage & Nazan, 2020.
"Wnt activation as a therapeutic strategy in medulloblastoma,"
Nature Communications, Nature, vol. 11(1), pages 1-12, December.
Handle:
RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17953-4
DOI: 10.1038/s41467-020-17953-4
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