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Human hepatocytes can give rise to intrahepatic cholangiocarcinomas

ABSTRACT: Human hepatocytes can give rise to intrahepatic cholangiocarcinomas

PROVIDER: PRJNA915042 | ENA |

REPOSITORIES: ENA

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Human hepatocytes can give rise to intrahepatic cholangiocarcinomas

Project description:To determine the transcriptomic similarity of undifferentiated carcinomas (UDCs) and intrahepatic cholangiocarcinomas (iCCAs) generated from primary human hepatocytes (phHeps) by oncogene expression and transplantation into immue-deficient mice with liver injury to iCCAs and hepatocellular carcinomas (HCCs) resected from patients.

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Transcriptomic signature of hepatocellular carcinoma and intrahepatic cholangiocarcinoma derived from oncogenically transformed murine hepatocytes

Project description:Primary liver cancer represents a major health problem. It comprises hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), which differ markedly with regards to their morphology, metastatic potential and therapy response. Yet, molecular actors and tissue context that commit transformed hepatic cells towards HCC or ICC are largely unknown. Here, we report that the hepatic microenvironment epigenetically shapes lineage commitment in mosaic mouse models of liver tumourigenesis. While a necroptosis associated hepatic cytokine microenvironment determines ICC outgrowth from oncogenically transformed hepatocytes, hepatocytes harbouring identical oncogenic drivers give rise to HCC if surrounded by apoptotic hepatocytes. Epigenome and transcriptome profiling of murine HCC and ICC singled out Tbx3 and Prdm5 as major microenvironment-dependent and epigenetically regulated lineage commitment factors, a function conserved in humans. Together, our study provides unprecedented insights into lineage commitment in liver tumourigenesis and explains molecularly why common liver damaging risk factors can either lead to HCC or ICC.

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Mutations in IDH1 and IDH2 are associated with DNA hypermethylation in intrahepatic cholangiocarcinomas

Project description:We compared the DNA methylation profiles of 12 intrahepatic cholangiocarcinomas harboring mutations in the genes encoding isocitrate dehydrogenase, IDH1 and IDH2, with 28 intrahepatic cholangiocarcinomas without these mutations. We profiled these samples with the Illumina HumanMethylation450 BeadChip, and characterized over 2,000 genes that were hypermethylated in tumors with mutations in IDH1 or IDH2.

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Expression data from murine intrahepatic biliary organoids

Project description:Mutations of isocitrate dehydrogenase (IDH) 1 or 2 occur in 10-30% of intrahepatic cholangiocarcinomas (ICCs). However, their functional roles in biliary carcinogenesis are still unknown. We used microarrays to investigate how mutant IDH1 affect the gene expression of intrahepatic biliary organoids generated from normal murine liver.

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Transcriptomic signature of hepatocellular carcinoma and intrahepatic cholangiocarcinoma derived from oncogenically transformed murine hepatocytes after stable knock-down of Tbx3 or Prdm5

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Mutations in IDH1 and IDH2 are associated with DNA hypermethylation in intrahepatic cholangiocarcinomas

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Autoimmunity and infection give rise to distict inflammatory Th17 subsets

Project description:Autoimmunity and infection give rise to distict inflammatory Th17 subsets

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DNA hypermethylation in intrahepatic cholangiocarcinomas and glioblastomas

Project description:This SuperSeries is composed of the following subset Series: GSE32079: Mutations in IDH1 and IDH2 are associated with DNA hypermethylation in intrahepatic cholangiocarcinomas GSE32283: Mutations in IDH1 are associated with DNA hypermethylation in glioblastomas Refer to individual Series

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Human hepatocyte metaplasia in injured humanized mouse livers

Project description:The goal of this experiment was to test whether human hepatocytes could give rise to biliary-like progenitor cells in an in vivo context. Here Fah-/- Il2ry-/- Rag2-/-NOD mouse livers were humanized with human hepatocytes. Only hepatocytes engraft in the Fah-/- mouse at detectable levels in this model. Then animals were given chronic liver injury with 0.1% ddc. After injury we measured human-specific transcripts to determine whether the phenotype of the human cells had changed. Specifically, we evaluated the relative levels of human biliary duct markers such as Spp1, Sox9, Krt7, etc. and hepatocyte markers such as Alb, Ttr, Fah, etc. 3 DDC treated chimeras and 6 untreated chimeras are included. Additional controls include a normal human liver biopsy, FACS sorted primary intrahepatic human bile duct cells, mouse hepatocytes, and mouse intrahepatic biliary cells in ddc treated animal.

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Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells

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