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.
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.
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.
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.
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.
Project description:Investigation of whole genome gene expression level changes of mRNAs and LncRNAs in portal vein tumor thrombus tissues and paired tumor tissues in hapatocellular carcinoma. The different expression genes were further analyzed.
