The β-catenin/WNT cell signaling pathway promotes the activation of gene transcription to mediate pleiotropic effects including cell growth and survival. The β-catenin/WNT signaling pathway is activated by the binding of the WNT1 ligand to a G-protein coupled receptor, frizzled (FZD1). The pathway is inhibited by the absence of the WNT1 ligand. 
Figure 1. In the presence of a WNT1 signal, disheveled (DVL1) induces the dissociation of the destruction complex. This causes the release of β-catenin, causing an increase in the levels of cellular β-catenin. Increased levels of β-catenin in the cell activate gene transcription and promote cell growth and survival. In the absence of a WNT1 signal, BTRC binds β-catenin, ubiquitinating β-catenin and marking it for degradation at the proteasome. Low levels of β-catenin in the cell cause the inhibition of gene transcription, cell growth, and survival. In cancer, the protein responsible for tagging β-catenin for ubiquitination is mutated. This allows for a constitutive increase in the levels of cellular β-catenin, causing uncontrolled cell growth and proliferation. Specific nodes in the pathway that are therapeutically actionable are noted.
Biomarkers in the beta-catenin/WNT signaling pathway serve as inclusion eligibility criteria in 18 clinical trials, of which 16 are open and 2 are closed. The genes APC, CTNNB1, WT1, BTRC, and DVL1 on this pathway most frequently harbor alterations that are inclusion eligibility criteria for clinical trials.
Of the trials that contain alteration(s) in the beta-catenin/WNT signaling pathway as inclusion criteria, 1 is n/a (1 open), 4 are phase 1 (3 open), 3 are phase 1/phase 2 (3 open), 6 are phase 2 (6 open), 1 is phase 2/phase 3 (1 open), 2 are phase 3 (1 open), and 1 is phase 4 (1 open) .