Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA309948 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CNV analysis of hepatocellular carcinoma with portal vein tumor thrombosis
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Project description:miRNA-seq analysis of hepatocellular carcinoma with portal vein tumor thrombosis
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Project description:RNA-seq analysis of hepatocellular carcinoma with portal vein tumor thrombosis
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Project description:The molecular landscape of hepatocellular carcinoma with portal vein tumor thrombosis
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Project description:Portal vein thrombosis (PVT) is a prevalent thrombotic complication in cirrhosis, yet its pathophysiology remains elusive, hindering effective treatment strategies. Unlike thrombosis in other vascular beds, anticoagulation often fails to achieve complete recanalization in PVT, highlighting the need of alternative therapeutic approaches. We investigated portal vein endothelium involvement in PVT pathogenesis, identifying potential therapeutic targets. We isolated for the first time primary human portal vein endothelial cells (PVEC) from explanted livers of cirrhotic patients with and without PVT, as well as from a control group without portal hypertension and conducted RNA sequencing. Transcriptomic analysis unveiled endothelial-to-mesenchymal transition (EndMT) pathway as a key mechanism underlying PVT in cirrhosis, predominantly induced through TGFβ/SMAD mechanism. Remarkably, coagulation markers remained unaffected. In silico drug repurposing identified statins as potential agents targeting these alterations. Our study elucidates significant endothelial changes in the portal vein of cirrhotic patients, particularly pronounced in those with PVT, with EndMT emerging as a pivotal process. Simvastatin emerges as a promising therapeutic option for PVT treatment and prevention by modulating EndMT in PVEC.
2025-12-02 | GSE261883 | GEO
Project description:Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear. We used microarrays to identify the functions of genes expressed in blood samples from patients with IPH. In order to examine the specific expression of genes in patients with IPH, we analyzed blood samples from three patients with IPH and three healthy volunteers as control using DNA microarrays.
2015-06-06 | E-GEOD-69601 | biostudies-arrayexpress
Project description:Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear. We used microarrays to identify the functions of genes expressed in blood samples from patients with IPH.
2015-06-06 | GSE69601 | GEO
Project description:Portal vein tumor thrombosis is a strong poor indication of HCC. Characterizing the molecular alterations of these metastatic HCCs is important for understanding the molecular mechanisms during HCC progression and metastasis. Previous genomic studies mainly focus on single molecular layer, such as gene expressions or exonic mutations. In this study, we systematically examined the copy number variation (CNV), DNA methylation, miRNA and transcriptome of matched adjacent normal tissues, primary tumors and PVTTs from 19 HCC patients. Based on the integrative multi-omics profiles, we established the molecular landscape of the metastatic HCCs and identified a set of the recurrent genomic alterations and candidate driver genes.
2017-02-17 | GSE77509 | GEO
Project description:Portal vein tumor thrombosis is a strong poor indication of HCC. Characterizing the molecular alterations of these metastatic HCCs is important for understanding the molecular mechanisms during HCC progression and metastasis. Previous genomic studies mainly focus on single molecular layer, such as gene expressions or exonic mutations. In this study, we systematically examined the copy number variation (CNV), DNA methylation, miRNA and transcriptome of matched adjacent normal tissues, primary tumors and PVTTs from 19 HCC patients. Based on the integrative multi-omics profiles, we established the molecular landscape of the metastatic HCCs and identified a set of the recurrent genomic alterations and candidate driver genes.
2017-02-17 | GSE76903 | GEO
Project description:Portal vein tumor thrombosis is a strong poor indication of HCC. Characterizing the molecular alterations of these metastatic HCCs is important for understanding the molecular mechanisms during HCC progression and metastasis. Previous genomic studies mainly focus on single molecular layer, such as gene expressions or exonic mutations. In this study, we systematically examined the copy number variation (CNV), DNA methylation, miRNA and transcriptome of matched adjacent normal tissues, primary tumors and PVTTs from 19 HCC patients. Based on the integrative multi-omics profiles, we established the molecular landscape of the metastatic HCCs and identified a set of the recurrent genomic alterations and candidate driver genes.
2017-02-17 | GSE77275 | GEO