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MiRNA profiling of biliary intraepithelial neoplasia reveals step-wise tumorigenesis in cholangiocarcinoma

ABSTRACT: miRNA profiling of biliary intraepithelial neoplasia reveals step-wise tumorigenesis in cholangiocarcinoma

PROVIDER: PRJNA587995 | ENA |

REPOSITORIES: ENA

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miRNA profiling of biliary intraepithelial neoplasia reveals step-wise tumorigenesis in cholangiocarcinoma

Project description:Biliary intraepithelial neoplasia (BilIN) is a common precursor lesion of distal cholangiocarcinoma (dCCA). However, the sequence leading from a single epithelial layer in normal biliary epithelia to intraepithelial precursor lesions and finally to the invasive tumor is poorly understood. Here, we aimed to elucidate key miRNAs involved in this stepwise process and to identify their possible mRNA target genes in distal cholangiocarcinogenesis. As basis of our study, we conducted Laser Capture Microdissection of FFPE tissue sections of 12 patients with distal cholangiocarcinoma. For each patient, we isolated three matched sample sets, including non-neoplastic biliary epithelia, high grade BilIN (grade 3), and invasive dCCA, thereby representing different stages of distal cholangiocarcinogenesis. This resulted in a total of 36 samples. Total RNA was extracted and the expression of ~800 miRNAs was assessed using the Nanostring® technology. Significantly deregulated miRNAs were validated by quantitative RT-PCR. Target genes were identified using miRWalk2.0 and validated by qRT-PCR and Western blot.

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miRNA profiling of biliary intraepithelial neoplasia reveals step-wise tumorigenesis in distal cholangiocarcinoma via the miR-451a/ATF2 axis

Project description:Distal cholangiocarcinoma (dCCA) is a biliary tract cancer with dismal prognosis and is often preceded by biliary intraepithelial neoplasia (BilIN) as a non-invasive precursor lesion. We found that miR-451a is downregulated in dCCA. Overexpression of mimic-451a in the CCA cell line SNU478 revealed multiple downregulated genes and potential miR-451a candidate targets.

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miRNA profiling of biliary intraepithelial neoplasia reveals step-wise tumorigenesis in distal cholangiocarcinoma via the miR-451a/ATF2 axis

Project description:miRNA profiling of biliary intraepithelial neoplasia reveals step-wise tumorigenesis in distal cholangiocarcinoma via the miR-451a/ATF2 axis

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Intraepithelial papillary neoplasia in the biliary tree is mediated by FGF10 signal

Project description:The new concept of neoplastic lesion of biliary tree, Biliary intraepithelial neoplasia (BilIN) and intraductal papillary neoplasm of bile duct (IPNB), as a conunterpart of pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neoplasm (IPMN), have been reported to be precancerous lesions in hilar and extrahepatic cholangiocarcinoma and arise from lining bile duct epithelium and peribiliary gland (PBG) under inflammation microenvironment in human. However, mouse model is lacking different from intrahepatic cholangiocarcinoma arised from canal of Hering in the liver. In a Doxycyclin-controlled transgenic mouse model of BilIN and IPNB, overexpression of Fibroblast Growth Factor 10 (FGF10) phenocopies human pathology with mutistep progression of cholangiocarcinogenesis in chronic cholangitis. The development and branching morphogenesis of BilIN and IPNB was induced by Fgf10/Erk signal and inhibited by MEK inhibiter. Pdx1+ PBG cells present in IPNB were able to lineage trace the early IPNB lesion as well as Krt19+ cholangiocytes. BiliN and IPNB with Kras mutation was irreversible different from no Kras mutation, and loss of p16 contributed to malignant transformation of BilIN and IPNB. Our data challenge the common paradigms regarding the pathogenesis of BilIN and IPNB.

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Project description:Transcriptome analysis of RNA samples from riboflavin deficiency combined with NMBA-induced rat esophageal intraepithelial neoplasia tissues. Epidemiological studies suggest that dietary riboflavin deficiency and environmental exposure to N-nitrosomethylbenzylamine (NMBA) are common in China's high incidence area of esophageal cancer. Riboflavin deficiency has been documented as an important risk factor for esophageal cancer. In this study, we established a F344 rat esophageal tumor model that combines dietary riboflavin deficiency with exposure to NMBA. The results showed that riboflavin deficiency combined with NMBA (R0N+) enhanced the incidence of esophageal intraepithelial neoplasia, including in situ carcinoma, whereas normal levels of riboflavin combined with NMBA (RcN+) mainly induced the occurrence of esophageal benign hyperplasia and small amount of esophageal intraepithelial neoplasia. Oxidative DNA damage (8-OHdG) and DNA double-strand breaks (p-γH2AX) in R0N+ rats were higher than that in RcN+ rats. The aim of the present study is to analyze the mechanism of riboflavin deficiency-induced tumorigenesis. So, we used Affymetrix Clariom D(also known as Rat Transcriptome Array 1.0) to identify genes that were differentially expressed upon R0N+ esophageal intraepithelial neoplasia tissues.

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Project description:Low grade flat ductal intraepithelial neoplasia (DIN1a, flat epithelial atypia) is one of the earliest morphologically recognizable neoplastic lesions of the breast. Frequently, it occurs in association with lobular intraepithelial neoplasia (LIN). The aim of this study was to elucidate chromosomal aberrations in these early neoplastic breast lesions using array comparative genomic hybridization (CGH) analysis. Laser capture microdissection of 12 archival formalin-fixed, paraffin-embedded specimens harbouring both foci of DIN1a as well as LIN was performed. All analyzed cases of DIN1a and LIN showed chromosomal gains and losses. The aberration encountered most often was loss on 16q in 7 DIN1a (70%) and 10 LIN (91%) cases. Regarding changes in chromosome 1, four DIN1a (40%) and 7 LIN (64%) cases showed a gain on 1q. The results of our study show concurrent chromosomal aberrations of 1q gains and 16q losses in several cases with coexisting LIN and low grade flat DIN. These aberrations are known to be common in low grade invasive ductal carcinomas as well as more advanced (conventional) types of low grade DIN (low grade ductal carcinoma in-situ). Our results raise the possibility of similar molecular-genetic pathways in most of the cases with coexisting LIN and low grade flat DIN.

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