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Wnt activation as a therapeutic strategy in medulloblastoma

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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    Cited by:

    1. Reza Mirzazadeh & Zaneta Andrusivova & Ludvig Larsson & Phillip T. Newton & Leire Alonso Galicia & Xesús M. Abalo & Mahtab Avijgan & Linda Kvastad & Alexandre Denadai-Souza & Nathalie Stakenborg & Ale, 2023. "Spatially resolved transcriptomic profiling of degraded and challenging fresh frozen samples," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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