Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hight througput RNA sequencing in a cohort of HBV related HCC and healty liver samples

ABSTRACT: RNA samples from matched tumour (T) and non tumour (NT, at least 2 cm distant from the T) tissues of 10 HBV-related HCC patients from 3 French clinical centres (Lyon Croix Rousse and Toulouse Hospitals and the French National Biological Resource Centres) have been retrospectively studied (Agreement DC-2008−235). RNAs from normal liver tissue samples of HBV, HCV and HIV negative adult patients undergoing lobectomy or segmental liver resection for medically required purposes unrelated to this research program at the Centre Leon Bérard (CLB) cancer center (ministerial agreements #AC-2013−1871 and DC-2013−1870) were used as controls. Signed informed written consents in compliance with the requirements of the local ethical committee were obtained from all patients before surgery.

ORGANISM(S): Homo sapiens

PROVIDER: GSE251942 | GEO | 2025/05/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of 32 human Anaplastic Large Cell Lymphomas (ALCL) and 5 ALCL cell lines to investigate differences between tumors expressing/not-expressing Anaplastic Lymphoma kinkase

Project description:A "Cartes d'Identite des Tumeurs" (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net). Affymetrix UU133A gene expression data for a series of 32 cases of systemic Anaplastic Large Cell Lymphoma (ALCL) and 5 ALCL cell lines; used to (1) confirm that tumors expressing Anaplastic Lymphoma Kinase (ALK+ ALCL) and ALK- ALCLs are different entities, (2) identify most significantly differentially expressed genes between ALK+ and ALK- samples, (3) generate a molecular signature of ALK- ALCL, (4) perform unsupervised analysis classifying ALCL in sub-groups related to morphology and clinical variables (e.g. disease stage and enrichment with 'early relapse' patients). Principal Investigator: Dr Georges DELSOL-- Centre de Physiopathologie Toulouse-Purpan CHU-Purpan -- Toulouse -- France -- Email: delsol.g@chu-toulouse.fr Programme "Cartes d'identite des Tumeurs" (CIT) of the "Ligue Nationale Contre le Cancer" (LNCC) Submitter: Fabien PETEL (petelf@ligue-cancer.net)

2007-05-05 | E-TABM-117 | biostudies-arrayexpress

PBMCs from stage IV melanoma patients after vaccination with melanoma-targeted mature dendritic cells (mDCs).

Project description:Patients affected by stage IV melanoma were subjected to a first round of DC vaccination in two centres, then PBMCs were extracted and mRNA analysed using Illumina arrays for identifying signals related to a favourable outcome of the therapy in terms of survival. A panel of candidate markers was further verified by real time PCR on PBMCs from patients treated with the same vaccination protocol in additional centres. This multi-centric study allowed to identify the gene PEBP1 as a candidate biomarker for vaccination positive outcome. The data released here was used to derive the first panel of markers.

2017-06-01 | E-MTAB-5201 | biostudies-arrayexpress

Analysis of the genome-wide distribution of RNA Pol II in a neuroblastoma cell line under silencing of RNA helicases DDX5 and DDX17

Project description:DEAD-box RNA helicases DDX5 and DDX17 regulate gene expression at different levels such as transcription and splicing, but the underlying mechanisms are not fully understood. A calibrated ChIP-seq analysis of total RNA Polymerase II was carried out in DDX5/DDX17-depleted SH-SY5Y cells to analyse the contribution of DDX5/DDX17 to RNAPII distribution. Univ Lyon, ENS de Lyon, CNRS UMR 5239, INSERM U1293, Laboratory of Biology and Modelling of the Cell, 46 Allée d'Italie, F-69007, Lyon, France. Corresponding author: cyril.bourgeois@inserm.fr

2022-08-04 | GSE183517 | GEO

Analysis of a neuroblastoma cell line transcriptome by polyA+ RNA sequencing under silencing of RNA helicases DDX5 and DDX17

Project description:DEAD-box RNA helicases DDX5 and DDX17 regulate gene expression at different levels such as transcription and splicing, but the underlying mechanisms are not fully understood. A transcriptome analysis of DDX5/DDX17-depleted human cells confirmed was carried out to further characterize the widespread deregulation of alternative splicing. This study also revealed a deregulation of 3’ end processing leading to transcriptional read-through. Univ Lyon, ENS de Lyon, CNRS UMR 5239, INSERM U1293, Laboratory of Biology and Modelling of the Cell, 46 Allée d'Italie, F-69007, Lyon, France. Corresponding author: cyril.bourgeois@inserm.fr

2022-08-04 | GSE183205 | GEO

HLA class I peptidome analysis of synthetic long peptide-fed human dendritic cells for therapeutic vaccine design

Project description:Synthetic long peptides (SLPs) are a promising vaccine modality that exploit dendritic cells (DC) to treat chronic infections or cancer. Currently, the design of SLPs relies on in silico prediction and multifactorial T cells assays to determine which SLPs are best cross-presented on DC human leukocyte antigen class I (HLA-I). Furthermore, it is unknown how TLR ligand-based adjuvants affect DC cross-presentation. Here, we generated a unique, high-quality immunopeptidome dataset of human DCs pulsed with 12 hepatitis B virus (HBV)-based SLPs combined with either a TLR1/2 (Amplivant®) or TLR3 (PolyI:C) ligand. The obtained immunopeptidome reflected adjuvant-induced differences, but no differences in cross-presentation of SLPs. We uncovered dominant (cross-)presentation on B-alleles, and identified 33 unique SLP-derived HLA-I peptides, several of which were not in silico predicted and some were consistently found across donors. Our work puts forward DC immunopeptidomics as a valuable tool for therapeutic vaccine design.

2025-01-19 | PXD051490 | Pride

The core cellular network modulates immune phenotype switching in hepatitis B

Project description:Hepatitis B virus (HBV) is a leading cause of liver-related diseases and mortality. However, immune mechanisms governing the phases of HBV infection remain elusive. Understanding molecular components in hepatitis immunosuppression and progression is essential for developing immunotherapies for functional cure of chronic HBV infection. Our integrative analysis of intrahepatic tissue and peripheral PBMC samples from patients with acute and chronic HBV infection using single-cell RNA sequencing (scRNA-seq) and TCR/BCR sequencing (scTCR/BCR-seq) revealed three distinct lineages of PBMC-derived intrahepatic T lymphocytes (hpCTLs): exhausted GZMK+PDCD1+, short-lived effector KLRG1+, and inactivated GZMB+PRF1+ hpCTLs. Key factors such as FasL/Fas-mediated cytotoxicity, CD28 co-stimulation, and exhaustion status were identified as determinants of hpCTL functionality. Liver-resident DC-SIGN+ macrophages were found to act as antigen-presenting cells that cross-prime hpCTLs in response to IL-2 or as suppressive macrophages by inhibiting T cell immunity through IL-10 and PD-L1 production and Treg recruitment. The intrahepatic core cellular network, including DC-SIGN+ macrophages, CSF1+ST2+ mast cells, AREG+ liver-resident NK cells, CD14+ hepatocytes, and CXCL13+ TFH, was observed to modulate immune tolerance, activation, and suppression in HBV infection. This study inferred the core cellular network involved in immune phenotype switching across different hepatitis B phases and suggested potential immunomodulatory strategies for treating chronic HBV infection.

2024-12-05 | GSE283471 | GEO

Genotyping data of French wild boar populations using a porcine genomic beadchip array

Project description:All-genome genotyping data from French wild boar populations could be useful for diversity studies in the wild boar species as well as for phylogeny studies with domestic pig populations. The data produced in this experiment concern 362 wild boars collected between 2013 and 2019 in various French departments. The biological samples that were collected were either blood samples or ear biopsies. Genomic DNA was extracted from cells after proteinase K lysis and ethanol precipitation. DNA was hybridized on the GeneSeek Genomic Profiler porcine beadchip (GGP70K HD Porcine Illumina) using Infinium technology. Fluorescence intensity data obtained for each Single Nucleotide Polymorphism were analyzed with GenomeStudio software to infer genotypes. In addition, the raw fluorescence data could be useful for Copy Number Variation studies.

2022-01-25 | E-MTAB-10591 | biostudies-arrayexpress

SLC38A2 and glutamine signaling in cDC1 dictate anti-tumor immunity [scRNA-Seq 2]

Project description:Cancer cells evade T-cell-mediated killing through poorly understood mechanisms of tumour–immune interactions. Dendritic cells (DCs), especially type-1 conventional DCs (cDC1), mediate T-cell priming and therapeutic efficacy against tumours. Besides pattern recognition receptors (PRRs), how DC functions are shaped by other environmental cues remains incompletely defined. Nutrients are emerging mediators of adaptive immunity, but whether nutrients impact DC function or innate–adaptive cell communication is largely unresolved. Here, we establish glutamine as an intercellular metabolic checkpoint to mediate tumour–cDC1 crosstalk and license cDC1 functionality for activating cytotoxic T cells. Intratumoral glutamine supplementation inhibits tumour growth by augmenting cDC1-mediated CD8+ T-cell immunity, and also overcomes therapeutic resistance to checkpoint blockade and T-cell-mediated immunotherapies. Mechanistically, tumour cells and cDC1 compete for glutamine uptake via transporter SLC38A2 to tune anti-tumour immunity. Nutrient screening and integrative analyses show that glutamine is the dominant amino acid for promoting cDC1 function, by signalling via FLCN to impinge upon TFEB function. Loss of FLCN in DCs selectively impairs cDC1 function in vivo in a TFEB-dependent manner, and phenocopies SLC38A2 deficiency by abrogating anti-tumour therapeutic effect of glutamine supplementation. Our findings establish glutamine-mediated intercellular metabolic crosstalk between tumour cells and cDC1 that underpins tumour immunoevasion, and reveal glutamine acquisition and signalling in cDC1 as limiting events for DC activation and putative targets for cancer treatment.

2023-05-24 | GSE210154 | GEO

SLC38A2 and glutamine signaling in cDC1 dictate anti-tumor immunity [scRNA-Seq 1]

2023-05-24 | GSE210153 | GEO

SLC38A2 and glutamine signaling in cDC1 dictate anti-tumor immunity [ATAC-Seq]

2023-05-24 | GSE210151 | GEO