Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

ABSTRACT: The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

PROVIDER: PRJNA894244 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

Project description:The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

| PRJNA898265 | ENA

The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

Project description:Adaptive immunotherapy including bispecific T cell engagers (TCE) has shown promise in the treatment of various cancers, but clinical responses are heterogeneous and often not durable. As response to TCE is suggested to be independent of tumor recognition and T cell state, molecular determinants or mediators of primary and acquired resistance towards TCE remain poorly understood. Here, we identify conserved behaviors of bone marrow residing CD4+ and CD8+ T cells in multiple myeloma patients undergoing TCE therapy. We show that the bone marrow immune landscape reacts to TCE therapy with cell state-dependent clonal T cell expansion and herewith infer coupling of tumor recognition via MHC-I, T cell exhaustion and clinical response. While we find the abundance of exhausted-like memory CD8+ T cell clones to be associated with clinical response failure, we describe loss of target epitope and MHC class I expression as tumor-intrinsic mechanisms of acquired resistance to TCE.

2022-10-28 | GSE216571 | GEO

The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

2023-03-09 | GSE217245 | GEO

Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma

Project description:Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma

| PRJNA922112 | ENA

Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [scTCRseq]

Project description:Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [scTCRseq]

| PRJNA923312 | ENA

Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [bulk RNAseq]

Project description:Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [bulk RNAseq]

| PRJNA913598 | ENA

Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [full scRNAseq]

Project description:Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [full scRNAseq]

| PRJNA922121 | ENA

Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [CD45 scRNAseq]

Project description:Response to tumor- infiltrating lymphocyte adoptive therapy is associated with preexisting CD8+T- myeloid cell networks in melanoma [CD45 scRNAseq]

| PRJNA914772 | ENA

Alternative Polyadenylation Determines the Functional Landscape of Inverted Alu Repeats

Project description:Alternative Polyadenylation Determines the Functional Landscape of Inverted Alu Repeats

| PRJNA972762 | ENA

Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer

Project description:The estrogen receptor alpha (ERa) drives the growth of two-thirds of all breast cancers. Endocrine therapy impinges on estrogen-induced ERa activation to block tumor growth. However, half of ERa-positive breast cancers are tolerant or acquire endocrine therapy resistance. Here we demonstrate that breast cancer cells undergo genome-wide reprogramming of their chromatin landscape, defined by epigenomic maps and chromatin openness, as they acquire resistance to endocrine therapy. This reveals a role for the Notch pathway while excluding classical ERa signaling. In agreement, blocking Notch signaling, using gamma-secretase inhibitors, or targeting its downstream gene PBX1 abrogates growth of endocrine therapy-resistant breast cancer cells. Moreover Notch signaling through PBX1 directs a transcriptional program predictive of tumor outcome and endocrine therapy response. Comparing histone modifications (H3K4me2 and H3K36me3), chromatin openness (FAIRE) and PBX1 binding between endocrine therapy sensitive MCF7 and resistant MCF7-LTED cells.

2013-05-01 | E-GEOD-37323 | biostudies-arrayexpress

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