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- W2779385611 abstract "// Rei Suzuki 1 , Hiroyuki Asama 1 , Yuichi Waragai 1 , Tadayuki Takagi 1 , Takuto Hikichi 2 , Mitsuru Sugimoto 1 , Naoki Konno 1 , Ko Watanabe 1 , Jun Nakamura 2 , Hitomi Kikuchi 2 , Yuki Sato 1 , Shigeru Marubashi 3 , Atsushi Masamune 4 and Hiromasa Ohira 1 1 Department of Gastroenterology, Fukushima Medical University School of Medicine, Fukushima, Japan 2 Department of Endoscopy, Fukushima Medical University Hospital, Fukushima, Japan 3 Department of Hepato-Biliary-Pancreatic and Transplant Surgery, Fukushima Medical University School of Medicine, Fukushima, Japan 4 Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan Correspondence to: Rei Suzuki, email: subaru@fmu.ac.jp Keywords: Pancreatic cancer; microRNA; fibrosis; digital PCR; chemotherapy Received: May 24, 2017 Accepted: November 29, 2017 Published: December 17, 2017 ABSTRACT We investigated whether serum microRNAs (miRNAs) could be diagnostic or prognostic markers in pancreatic ductal adenocarcinoma (PDAC). We first identified miRNAs showing altered expression in human pancreatic stellate cells (hPSCs) co-cultured with PDAC cells (Panc-1 and BxPC-3) as compared to hPSCs cultured alone. Among the miRNAs with altered expression, let-7d exhibited reduced expression in an in silico analysis of The Cancer Genome Atlas data. Inhibition of let-7d resulted in enhanced expression of fibrosis-related genes. We extracted serum miRNA from 45 PDAC patients and 42 healthy controls and quantified expression let-7d using digital PCR. Based on the level of let-7d expression, we were able to distinguish between PDAC patients and controls. Additionally, reduced let-7d expression correlated with poor overall survival. Thus, fibrosis-related miRNAs may be serum biomarkers for PDAC." @default.
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- W2779385611 date "2017-12-17" @default.
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- W2779385611 title "Fibrosis-related miRNAs as serum biomarkers for pancreatic ductal adenocarcinoma" @default.
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- W2779385611 doi "https://doi.org/10.18632/oncotarget.23377" @default.
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