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摘要: Wilms tumor (WT) is the most common renal neoplasm of childhood and affects 1 in 10,000 children aged less than 15 years. These embryonal tumors are thought to arise from primitive nephrogenic rests that derive from the metanephric mesenchyme during kidney development and are characterized partly by increased Wnt/β-catenin signaling. We previously showed that coordinate activation of Ras and β-catenin accelerates the growth and metastatic progression of a murine WT model. Here, we show that activating KRAS mutations can be found in human WT. In addition, high levels of phosphorylated AKT are present in the majority of WT’s. We further show in a mouse model and in renal epithelial cells that Ras cooperates with β-catenin to drive metastatic disease