Frequent RNF43 mutation contributes to moderate activation of Wnt signaling in colorectal signet-ring cell carcinoma

Abstract

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Clinicopathological features of tumor mutation burden, Epstein-Barr virus infection, microsatellite instability and PD-L1 status in Chinese patients with gastric cancer

“…RNF43 mutation results in a frame shift that leads to the early truncation and potential inactivation of the associated protein, and as such, may be a predictor of pathogenesis [ 32 ]. Yu et al discovered a high frequency of RNF43 mutations in colorectal signet ring cell carcinoma, and that mutated RNF43 activates the Wnt pathway [ 33 ]. As with RNF43, frame shift mutations in the BRCA2 gene lead to the early truncation of the protein, and its subsequent inactivation may predict pathogenesis.…”

Clinicopathological features of Epstein-Barr virus infection, microsatellite instability, tumor mutation burden and PD-L1 status in Chinese patients with gastric cancer

“…Preclinical studies of gastric and colorectal cancer have shown that the inactivation of RNF43 promotes cellular proliferation and tumor growth [33]. Yu et al discovered a high frequency of RNF43 mutations in colorectal signet ring cell carcinoma, and that mutated RNF43 activates the Wnt pathway [34]. As with RNF43, frame shift mutations in the BRCA2 gene lead to the early truncation of the protein, and its subsequent inactivation may predict pathogenesis.…”

Clinicopathological Features of Epstein-Barr Virus Infection, Microsatellite Instability, Tumor Mutation Burden and PD-L1 Status in Chinese Patients with Gastric Cancer

“…RNF43 mutation results in a frame shift that leads to the early truncation and potential inactivation of the associated protein, and as such, may be a predictor of pathogenesis [33]. Yu et al discovered a high frequency of RNF43 mutations in colorectal signet ring cell carcinoma, and that mutated RNF43 activates the Wnt pathway [34]. As with RNF43, frame shift mutations in the BRCA2 gene lead to the early truncation of the protein, and its subsequent inactivation may predict pathogenesis.…”