Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq 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: GSE77509 | GEO | 2017/02/17

SECONDARY ACCESSION(S): PRJNA310654

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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.

2017-02-17 | GSE77275 | GEO

DNA methylation analysis of hepatocellular carcinoma with portal vein tumor thrombosis

2017-02-17 | GSE77269 | GEO

miRNA-seq analysis of hepatocellular carcinoma with portal vein tumor thrombosis

2017-02-17 | GSE76903 | GEO

The molecular landscape of hepatocellular carcinoma with portal vein tumor thrombosis

Project description:The molecular landscape of hepatocellular carcinoma with portal vein tumor thrombosis

| PRJNA309945 | ENA

Microarray analysis of microRNA expression patterns in different hepatocellular cancinoma subtypes

Project description:Previously, we have found a specific subtype of HCCs named solitary large hepatocellular carcinoma (SLHCC), which was >5 cm in diameter, had just single lesion, and always grew expansively within an intact capsule or pseudocapsule. Accordingly, we classified HCCs into 3 different subtypes: SLHCC, nodular HCC (NHCC, node number ≥ 2) and small HCC (SHCC, solitary nodular, diameter ≤ 5 cm). Further study confirmed that SLHCC had unique clinical and pathological characteristics, and its metastatic potential was comparable with SHCC, but significantly lower than NHCC. After hepatic resection, SLHCC exhibited a similar long-term overall and disease-free survival with SHCC, but much better than NHCC. To gain a better understanding of the molecular biologic characteristics of SLHCC, we performed miRNAs array analysis in there three subtypes of HCC.

2015-05-01 | E-MTAB-3347 | biostudies-arrayexpress

A targetable pathway in neutrophils mitigates both arterial and venous thrombosis

Project description:Arterial and venous (A/V) thrombosis constitutes the greatest source of morbidity and mortality worldwide. Long considered as distinct entities, accumulating evidence indicates that A/V thrombosis can occur in the same populations suggesting that common mechanisms are likely operative. Although hyperactivation of the immune system is a common forerunner to the genesis of thrombotic events in both vascular systems, the key molecular control points remain poorly understood. Consequently, anti-thrombotic therapies targeting the immune system for therapeutic gain are lacking. Here we show that neutrophils are key effectors of both A/V thrombosis and can be targeted via novel immunoregulatory nanoparticles. Using antiphopholipid antibody syndrome (APS) as a model for devastating A/V thrombosis, we identified the transcription factor Krüppel-like factor 2 (KLF2) as a key regulator of neutrophil activation. Upon activation via genetic loss of KLF2 or administration of antiphospholipid antibodies, neutrophils cluster P-selectin glycoprotein ligand 1 (PSGL-1) via cortical actin remodeling, thereby increasing adhesion potential at thrombosis sites. Targeting clustered PSGL-1 using designer nanoparticles attenuates neutrophil-mediated A/V thrombosis in APS and KLF2 knockout models, illustrating the importance and feasibility of targeting activated neutrophils to prevent pathological thrombosis. Together, our results demosntrate a role for activated neutrophils to prevent pathological thrombosis. Together, our results demonstrate a role for activated neutorphils in both arterial and venous thrombosis and identify key molecular events that serve as potential targets for therapeutics against diverse causes of immunothrombosis.

2022-09-12 | GSE208336 | GEO

Single-cell RNA sequencing on the vein wall of mouse deep vein thrombosis

Project description:Deep vein thrombosis (DVT) is a common clinical problem, but its cellular and molecular mechanisms remain incompletely understood. We performed single-cell RNA sequencing (scRNA-seq) on the vein wall of mouse inferior vena cava (IVC) ligation model of deep vein thrombosis (DVT), to analyze the transcriptomic changes in the vein wall during acute venous thrombosis.

2023-02-10 | GSE221978 | GEO

Expression profiles of hepatocellular carcinomas derived from ductular progenitor cells

Project description:Hepatocellular carcinoma (HCC) generally arises in chronically inflamed liver and is thought to originate from regenerating liver cells that acquired genetic alterations. Both hepatocytes and ductular progenitor cells (DPCs) contribute to liver regeneration and are candidate cellular origins of HCCs. In the current study, we used lineage-tracing analysis to show that Epcam-expressing DPCs give rise to HCCs in inflamed liver. Under conditions in which proliferating DPCs differentiate into cholangiocytes but not into hepatocytes, the accumulation of genetic alterations in Epcam-expressing DPCs resulted in the development of HCCs with histologic features of concomitant ductule-like structures resembling human cholangiolocellular carcinoma (CLC). To elucidate the characteristics of DPC-derived HCC, gene expression of HCCs derived from Epcam-expressing DPCs were evaluated using Agilent SurePrint G3 Mouse Gene Expression 8x60K v2. Two DPC-derived HCCs with CLC components, two DPC-derived HCCs without CLC, and two HCCs derived from albumin-expressing cells were analyzed.

2020-02-19 | GSE95099 | GEO

Vascular Disease and Thrombosis in SARS-CoV-2 Infected Humans and Rhesus Macaques

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.

2020-10-20 | GSE156701 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data