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- W4311802169 abstract "Pancreatic cancer (PC) is one of the most dismal diseases with a five-year survival rate of only 6%. Such poor prognosis is attributed to both a lack of early detection methods and its intrinsic resistance to cytotoxic agents and radiotherapy. Identifying driving events in the initial stage is of great significance for curable pancreatic ductal adenocarcinoma (PDA) detection and effective targeted therapy. Furthermore, Kirsten rat sarcoma viral oncogene (KRAS) plays a critical role in the initiation and maintenance of pancreatic tumors, thus contributing to the conversion of anti-tumor inflammation to pro-tumor inflammation. Both the KRAS mutation and inflammation are concurrent in the initial stage of PDA, and they compose a positive feedback loop to enhance each other’s activity. This positive feedback loop generates a harsh environment, which helps pancreatic cells maintain the stemness phenotype, accelerates cell turnover rate, increases genome instability, and hence elevates the incidence of PDA formation." @default.
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- W4311802169 date "2022-11-16" @default.
- W4311802169 modified "2023-10-05" @default.
- W4311802169 title "The Positive Feedback Loop Between Inflammation and Mutant KRAS Genes Promotes Malignant Transformation in Chronic Pancreatitis" @default.
- W4311802169 doi "https://doi.org/10.14218/csp.2022.00012" @default.
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