p53 Loss Rearranges Wnt Signaling Spatial Gradients to Drive Mutant Cells Into Normal Tissue

A collaborative study by the Icahn School of Medicine at Mount Sinai and the Fred Hutchinson Cancer Center, published in Science, found that loss of p53 function not only upregulates growth pathway activity but also reorganizes the Wnt signaling pathway. Wnt signaling was weaker at the edges of mutant cell clones and stronger at their centers, and this radial spatial gradient was closely linked to efficient expansion of mutant clones.