The abstract reports both gain-of-function and loss-of-function CTNNB1 mutations are detected in human cancers, presenting a paradox. Understanding this dual role is critical for developing targeted therapies and predicting treatment responses in β-catenin-driven diseases. Gap type: contradiction Source paper: Multi‑layered prevention and treatment of chronic inflammation, organ fibrosis and cancer associated with canonical WNT/β‑catenin signaling activation (Review). (None, None, PMID:29786110)
Landscape Summary: What mechanisms explain how β-catenin mutations can be both oncogenic and tumor suppressive in cancer? is a 0.8 priority gap in cancer-biology. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
What mechanisms explain how β-catenin mutations can be both oncogenic and tumor suppressive in cancer? — INVOKE-2 (completed)
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