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DNA methylation analysis of hepatocellular carcinoma with portal vein tumor thrombosis

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE77269 | GEO | 2017/02/17

SECONDARY ACCESSION(S): PRJNA309948

REPOSITORIES: GEO

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CNV analysis of hepatocellular carcinoma with portal vein tumor thrombosis

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.

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Project description:The COVID-19 pandemic has led to extensive morbidity and mortality throughout the world. Clinical features that drive SARS-CoV-2 pathogenesis in humans include inflammation and thrombosis, but the mechanistic details that underlie these processes remain to be determined. In this study, we demonstrate endothelial disruption and vascular thrombosis in histopathologic sections of lungs from both humans and rhesus macaques infected with SARS-CoV-2. To define key molecular and cellular pathways associated with SARS-CoV-2 pathogenesis, we performed transcriptomic analyses of bronchoalveolar lavage (BAL) samples and peripheral blood, and proteomics analyses of serum from infected rhesus macaques. We observed upregulation of macrophage signatures, complement cascade pathways, platelet activation, and markers of thrombosis in BAL and peripheral blood as well as extensive macrophage infiltrates in lung. These observations coincided with robust induction of interferon and proinflammatory markers, including C-reactive protein, MX1, IL-6, IL-1, IL-8, TNFa and NF-κB as well as downstream signaling pathways. These findings suggest a model in which critical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2 induced vascular disease. Our findings also suggest potential novel therapeutic targets for COVID-19 disease.

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Portal vein thrombosis.

Project description:Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion.

| S-EPMC4415192 | biostudies-other

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