Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single T-cell receptor profiling identifies distinct patterns of T-cell infiltration in nodal B-cell lymphoma entities

ABSTRACT: The redirection of T-cells has emerged as an attractive therapeutic principle in B-cell non-Hodgkin lymphoma (B-NHL). However, a detailed characterization of lymphoma-infiltrating T-cells across B-NHL entities is missing. Here, we present single-cell transcriptome and T-cell receptor sequencing of lymph-node derived T-cells from patients with diffuse large B-cell, mantle cell, follicular, or marginal zone lymphoma, and from healthy controls. These data revealed quantitative aberrations of the T-cell microenvironment across and within B-NHL entities.

ORGANISM(S): Homo sapiens

PROVIDER: GSE252455 | GEO | 2024/01/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Multimodal single-cell profiling identifies distinct patterns of T-cell infiltration in nodal B-cell lymphoma entities

Project description:The redirection of T-cells has emerged as an attractive therapeutic principle in B-cell non-Hodgkin lymphoma (B-NHL). However, a detailed characterization of lymphoma-infiltrating T-cells across B-NHL entities is missing. Here, we present cellular indexing of transcriptomes and epitopes of lymph-node derived T-cells from patients with diffuse large B-cell, mantle cell, follicular, or marginal zone lymphoma, and from healthy controls. These data revealed quantitative aberrations of the T-cell microenvironment across and within B-NHL entities.

2024-01-28 | GSE252608 | GEO

Kinome profiling of Non-Hodgkin Lymphoma identifies Tyro3 as a therapeutic target in PEL

Project description:Non-Hodgkin lymphomas (NHL) make up the majority of lymphoma diagnoses and represent a very diverse set of malignancies. We sought to identify kinases uniquely upregulated in different NHL subtypes. Using Multiplexed Inhibitor Bead-mass spectrometry (MIB/MS), we found Tyro3 was uniquely upregulated and important for cell survival in primary effusion lymphoma (PEL), which is a viral lymphoma infected with Kaposi’s sarcoma-associated herpesvirus (KSHV).

2019-07-11 | PXD012087 | Pride

Gene knock down studies revealed CCDC50 as candidate gene in mantle cell lymphoma and chronic lymphocytic leukemia

Project description:The two B-cell non-Hodgkin lymphoma (NHL) entities chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) show recurrent chromosomal gains of 3q25 q29, 12q13 q14 and 18q21-q22. The pathomechanisms affected by these aberrations are not understood. The aim of this study was to identify genes, located within these gained regions, which control cell death and cell survival of MCL and CLL cancer cells. Blood samples from 24 CLL and 6 MCL patients as well as 6 cell lines representing both malignancies were analyzed by gene expression profiling. By comparison of genomic DNA and gene expression, 72 candidate genes were identified. We performed a limited RNAi screen with these candidates in order to identify genes affecting cell survival. CCDC50, SERPINI2 and SMARCC2 mediated a reduction of cell viability in primary CLL cells as well as in cell lines. Gene knock down and a NFkB reporter gene assay revealed that CCDC50 is required for survival in MCL and CLL cells and controls NFkB signaling. This SuperSeries is composed of the SubSeries listed below.

2010-06-03 | GSE16413 | GEO

Gene expression data in obinuzumab treated Karpas-1106P PMBL cell line

Project description:Primary Mediastinal large B-cell lymphoma (PMBL) is a rare form of non-Hodgkin lymphoma (NHL) representing 2% of mature B-cell NHL in patients less than 18 years of age.We compared the gene expression profiling between fully humanized anti-CD20 targeted monoclonal antibody recognizing a unique CD20 type II epitope, obinutuzumab and IgG or PBS treated Karpas Primary Mediastinal B-cell lymphoma (PMBL) cell line. -

2016-12-01 | GSE75605 | GEO

Microarray-based CGH in human lymphoma cell lines.

Project description:This series represents the data set of Array CGH from the paper (submit for publication): “Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas. Mestre et all. ” and it's web supplement. The molecular nature of many secondary events in the pathogenesis of B-cell non Hodgkin lymphoma (B-NHL) remains unknown. We used high-resolution CGH to BAC microarrays to characterize the genomes of 48 B-cell non-Hodgkin lymphoma (B-NHL) cell lines of different origins. Array CGH identified, on average, 20 genomic alterations per cell line, including regional gains and losses as well as previously uncharacterized aberrations. Different genomic patterns were observed among the B-NHL subtypes. To search for possible oncogenic target genes, gene expression profiling was performed in the cell lines models. Integrative genomic and gene expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored. Array-based comparative genomic hybridization (CGH) and gene expression microarray analysis of 48 cell lines derived from patients with different B-NHLs delineated twenty homozygous deletions at seven chromosome areas, all of which contained tumor suppressor gene targets. Further investigation revealed that only a fraction of primary biopsies presented inactivation of these genes by point mutation or intragenic deletion, but instead some of them were frequently silenced by epigenetic mechanisms. Our microarray strategy has identified novel candidate suppressors inactivated by genetic and epigenetic mechanisms that substantially vary among the B-NHL subtypes. Keywords: Array CGH, B-cell non-Hodgkin lymphoma, genomic amplification, homozygous deletion

2007-02-05 | GSE5316 | GEO

Multimodal single-cell profiling identifies distinct patterns of T-cell infiltration in nodal B-cell lymphoma entities

Project description:Multimodal single-cell profiling identifies distinct patterns of T-cell infiltration in nodal B-cell lymphoma entities

| PRJNA1061512 | ENA

Molecular and pathological characterisation of diffuse large B-cell lymphomas in children with Nijmegen breakage syndrome

Project description:Nijmegen-breakage syndrome (NBS, OMIM #251260) is an autosomal recessive chromosomal instability syndrome characterized by a very distinct phenotype (microcephaly, growth retardation, immunodeficiency) associated with increased predisposition to develop malignancies, particularly of lymphoid origin (by the age of 20 years, over 40% of NBS patients develop cancer). Immunological lineage of lymphomas in NBS significantly differs from Non-Hodgkin Lymphomas (NHL) entities observed in general pediatric population as well as in primary immunodeficiencies. There is a strong predominance of diffuse large B-cell lymphoma (DLBCL) and T cell lymphoblastic lymphoma (T-LBL/ALL), all showing clonal Ig/TCR rearrangements. In the current study we aimed to examined gene expression signature of metabolic pathways in DLBCL cells.

2024-08-23 | GSE213555 | GEO

Homo sapiens

Project description:CGCI: Non-Hodgkin Lymphoma (NHL)

| PRJNA172563 | ENA

Single T-cell receptor profiling identifies distinct patterns of T-cell infiltration in nodal B-cell lymphoma entities

Project description:Single T-cell receptor profiling identifies distinct patterns of T-cell infiltration in nodal B-cell lymphoma entities

| PRJNA1060684 | ENA

Activity of the novel BTK inhibitor TG-1701 is associated with the disruption of the Ikaros signaling pathway in responder B-NHL patients and with sensitization to anti-CD20 therapy in B-NHL xenografts

Project description:Covalent Bruton's tyrosine kinase inhibitors (BTKis) have transformed the treatment of B-cell non-Hodgkin lymphoma (B-NHL), including chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL), but their activity has been limited by off-target toxicity and acquired drug resistance. TG-1701 is a novel irreversible and highly specific BTKi being presently under study in a phase 1 clinical trial in patients with relapsed/refractory B-NHL alone and in combination with ublituximab, a CD20 antibody, and umbralisib, a dual PI3Kδ and CK1ε inhibitor. Here we show, for the first time that phosphoproteomic analysis of CLL patients receiving a BTKi (TG-1701) led to a non-supervised clustering that matched the clinical outcomes and separated a group of “responders” from a group of “non-responders”. This clustering was based on a selected list of 96 phosphosites, with Ikaros-Ser442/445 phosphorylation as a potential marker for TG-1701 efficacy. RNA-seq analysis followed by qPCR and western blot validation further revealed that TG-1701 treatment blunted the Ikaros gene signature only in responder patients, as well as in BTKi-sensitive, but not BTKi-insensitive, B-NHL cell lines and xenografts. Importantly, and in contrast with ibrutinib, TG-1701 did not impair FcγR-driven antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP) triggered by the anti-CD20 antibodies rituximab and ublituximab in a multicellular MCL co-culture system. In addition, TG-1701 cooperated with ublituximab coupled to umbralisib (also referred as the U2 regimen) in reducing the tumor growth in both ibrutinib-sensitive and ibrutinib-insensitive mouse models of MCL. Altogether, these data validate phosphoproteomic as a broken thread to omics analysis in the clinic and support the use of TG-1701-U2 combination in R/R B-NHL patients, irrespective of prior response to ibrutinib.

2021-09-22 | PXD023231 | Pride

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