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Epigenetic footprint of hepatoblastoma defines a novel integrative molecular classification with clinical implications [Infinium MethylationEPIC]

ABSTRACT: Hepatoblastoma (HB) is the predominant pediatric liver cancer with limited therapeutic options for patients with aggressive tumors. Nevertheless, it is a rare disease. Here, we performed a high-throughput molecular study of 32 patients with HB and major findings were validated in additional 80 cases. We unveiled an epigenetic footprint including downregulation of RNA-editing, hyperediting of the tumor suppressor BLCAP,14q32 DLK1-DIO3 locus overexpression, DNA hypomethylation and CpG island hypermethylation. Based on these findings, we defined an integrative molecular classification of HB that improve current clinical stratification, and identified CHKA as a therapeutic target for the poor prognostic subclass.

ORGANISM(S): Homo sapiens

PROVIDER: GSE132399 | GEO | 2020/07/09

REPOSITORIES: GEO

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Epigenetic footprint of hepatoblastoma defines a novel integrative molecular classification with clinical implications [CytoScanHD_Array]

Project description:Hepatoblastoma (HB) is the predominant pediatric liver cancer with limited therapeutic options for patients with aggressive tumors. Nevertheless, it is a rare disease. Here, we performed a high-throughput molecular study of 32 patients with HB and major findings were validated in additional 80 cases. We unveiled an epigenetic footprint including downregulation of RNA-editing, hyperediting of the tumor suppressor BLCAP,14q32 DLK1-DIO3 locus overexpression, DNA hypomethylation and CpG island hypermethylation. Based on these findings, we defined an integrative molecular classification of HB that improve current clinical stratification, and identified CHKA as a therapeutic target for the poor prognostic subclass.

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Project description:To understand molecular mechanisms driving HB pathogenesis, we hypothesize that pathologic activation of Enhancer of Zeste Homolog 2 contributes to hepatoblastoma propagation. Here we demonstrate that EZH2 promotes proliferation in HB cell lines through interaction with β-catenin, the most frequently mutated gene in HB. We demonstrate that canonical and noncanonical EZH2 signaling occur in HB tumor cells, likely driven by aberrant EZH2 expression. We use comparison groups of liver cancer, hepatocytes, and dermal fibroblasts to establish the hepatoblastoma identity of our patient-derived cell lines.

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Project description:Hepatoblastoma (HB) is the most common pediatric liver cancer. Its exclusive occurrence in very young children leads us to investigating whether the immature liver provides a protumorigenic niche to HB development. We employed the single-cell RNA-sequencing (sc-RNAseq) to comprehensively profile the HB tumors and their microenvironment in the orthotopic transplantation models established in postnatal day 5 and 60. We demonstrated that the neonatal liver provides a prometastatic niche to HB development via Cxcl1/Cxcr2 axis-mediated HB-aHSC interaction.

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Epigenetic footprint of hepatoblastoma defines a novel integrative molecular classification with clinical implications [Infinium MethylationEPIC]

Project description:Epigenetic footprint of hepatoblastoma defines a novel integrative molecular classification with clinical implications [Infinium MethylationEPIC]

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Genomic Copy-Number Variations in Hepatoblastoma Patients Revealed by Array Comparative Genomic Hybridization

Project description:Purpose: Hepatoblastoma (HB) is a malignant pediatric hepatic progenitor cell tumor with uncertain etiology. To discover genomic biomarkers associated with this malignancy, we conduct the study. Experimental Design: A panel of ten cases and two pairs of identical twins for HB were screened using high-resolution array-based comparative genomic hybridization (array CGH) technology. Genomic DNA from the peripheral blood was subject to our laboratory investigation. Results: In total of the twelve HB cases tested, we identified four high recurrent copy-number variations (CNVs) including gain on 1p13.3 (25%) and losses on 5p15.33 (33.3%), 16q12.2 (33.3%), and 19q13.42 (25%). Additionally, the twin study indicated that microdeletions of 3p12.1 and 12p13.2 correlated with hepatoblastoma occurrence. Among these candidate CNVs, 5p15.33 and 16q12.2 not only the most prevalent genomic deletion in this survey, but also encompassed hepatic expressed gene, Zinc finger, DHHC-type containing 11B (ZDHHC11B) and Zinc finger, DHHC-type containing 11 (ZDHHC11) map to 5p15.33; carboxylesterase 4-like (CES4) map to 16q12.2. Furthermore, the microdeletion of 5p15.33 was associated with high mortality rate (3/3; P = 0.018) in patients with native liver. Currently, the only surviving patient with 5p15.33 microdeletion is who has receipt liver transplantation. Conclusions: These results suggested that losses on 3p12.1, 5p15.33, 12p13.2 and 16q12.2 may be pathogenic for HB. In addition, HB patient who affected by 5p15.33 microdeletion seems to carry high risk of mortality unless undergo liver transplantation. Thus, 5p15.33 microdeletion was suggested as potential prognostic biomarker for poor survival in hepatoblastoma.

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Project description:Forty-nine hepatoblastoma (HB) tumor specimens were profiled on a microarray containing 250human miRNA, in order to identify miR classifiers that could discriminate HBs with diverse prognosis, and to get insight on the functional mechanisms in which miRNAs are involved. Hierarchical unsupervised clustering of HB samples according to their miRNA expression profile identifies 2 tumor subgroups associated with different degree of differentiation, proliferation rate and invasive phenotype. As subset of these tumors is used as training set to build a mir classifier. When the signature is applied to an independent test set, an independent series of HB is classified patients into two groups associated with the clinical features identified in the first set of patients.

2011-07-08 | E-GEOD-20971 | biostudies-arrayexpress

miRNA expression of human samples of hepatoblastoma (HB) and normal and fetal liver

2011-07-08 | GSE20971 | GEO

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