Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [ATAC-seq]

ABSTRACT: CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [ATAC-seq]

PROVIDER: PRJNA815055 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR18300812_1.fastq.gz	Fastqsanger.gz
	SRR18300812_2.fastq.gz	Fastqsanger.gz
	SRR18300813_1.fastq.gz	Fastqsanger.gz
	SRR18300813_2.fastq.gz	Fastqsanger.gz
	SRR18300814_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas

Project description:CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas

| PRJNA815051 | ENA

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [scRNA-seq]

Project description:CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [scRNA-seq]

| PRJNA815054 | ENA

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [scRNA-seq]

Project description:Purpose: We show that genetic ablation or pharmacological inhibition of H3K9-methyl transferase Suv39h1 delays tumor growth and potentiates tumor rejection by anti-PD-1.

2022-03-14 | GSE198422 | GEO

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas [ATAC-seq]

Project description:Purpose: We show that genetic ablation or pharmacological inhibition of H3K9-methyl transferase Suv39h1 delays tumor growth and potentiates tumor rejection by anti-PD-1.

2022-03-14 | GSE198421 | GEO

CD8+T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas.

Project description:Tumor-infiltrating CD8 + T cells progressively lose functionality and fail to reject tumors. The underlying mechanism and re-programing induced by checkpoint blockers are incompletely understood. We show here that genetic ablation or pharmacological inhibition of histone lysine methyltransferase Suv39h1 delays tumor growth and potentiates tumor rejection by anti-PD-1. In the absence of Suv39h1, anti-PD-1 induces alternative activation pathways allowing survival and differentiation of IFNγ and Granzyme B producing effector cells that express negative checkpoint molecules, but do not reach final exhaustion. Their transcriptional program correlates with that of melanoma patients responding to immune-checkpoint blockade and identifies the emergence of cytolytic-effector tumor-infiltrating lymphocytes as a biomarker of clinical response. Anti-PD-1 favors chromatin opening in loci linked to T-cell activation, memory and pluripotency, but in the absence of Suv39h1, cells acquire accessibility in cytolytic effector loci. Overall, Suv39h1 inhibition enhances anti-tumor immune responses, alone or combined with anti-PD-1, suggesting that Suv39h1 is an "epigenetic checkpoint" for tumor immunity.

| S-EPMC9243005 | biostudies-literature

CD8+ T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-14 | GSE198423 | GEO

Expression data in PD-L1 positive and PD-L1 negative human melanoma samples

Project description:Blocking the PD-1/PD-L1 immunosuppressive pathway has shown promise in the treatment of certain cancers including melanoma. This study investigates differences in the gene expression profiles of human melanomas that do or do not display the immunosuppressive protein PD-L1. Further understanding of genes expressed within the tumor microenvironment of PD-L1+ tumors may lead to improved rationally designed treatments. Gene expression profiling was performed on total RNA extracted by laser capture microdissection from 11 archived formalin-fixed paraffin-embedded (FFPE) melanoma specimens, 5 of which were PD-L1 positive and 6 PD-L1 negative. Details of the design, and the gene signatures found are given in the paper associated with this GEO Series: Janis M. Taube, Geoffrey D. Young, Tracee L. McMiller, Shuming Chen, January T. Salas, Theresa S. Pritchard, Haiying Xu, Alan K. Meeker, Jinshui Fan, Chris Cheadle, Alan E. Berger, Drew M. Pardoll, and Suzanne L. Topalian, Differential expression of immune-regulatory genes associated with PD-L1 display in melanoma: implications for PD-1 pathway blockade, Clin Cancer Res 2015, in press.

2015-05-01 | E-GEOD-65041 | biostudies-arrayexpress

Effects of SUV39H1 depletion on gene expression in HeLa cells

Project description:HeLa cells were transiently transfected with siRNA against SUV39H1, a histone H3K9 methyltransferase. Several genes were significantly up- or down-regulated. HeLa cells were transiently transfected with siRNA against SUV39H1 or negative control siRNA. Then total RNA was extracted.

2015-08-01 | E-GEOD-59243 | biostudies-arrayexpress

Expression data in PD-L1 positive and PD-L1 negative human melanoma samples

2015-05-01 | GSE65041 | GEO

Expression data from Adriamycin-treated Emu-myc; Suv39h1-/- B-cell lymphoma

Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.

2013-07-04 | E-GEOD-44355 | 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