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. 2019 Sep 28;69(6):1092–1103. doi: 10.1136/gutjnl-2019-319126

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See: https://creativecommons.org/licenses/by/4.0/.

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Model of Wnt negative regulation in ligand-dependent (LD) and ligand-independent (LI) tumours. In LD tumours, mutations in the synergistic RSPO axis upregulate Wnt signalling through an otherwise intact canonical Wnt signalling pathway. In this situation, appropriate upregulation of Wnt NRs (blue shapes) could restrain pathological Wnt pathway activity which generates a selective pressure for targeted methylation and epigenetic suppression of key Wnt NR activity (red borders). In LI tumours, downstream mutation in APC and CTNNB1 causes constitutive activation of Wnt intracellular signalling pathways rendering Wnt negative feedback functionally redundant and disconnecting the physiological negative regulator equilibrium.