Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance

ABSTRACT: MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance

PROVIDER: PRJNA862161 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR20634119_1.fastq.gz	Fastqsanger.gz
	SRR20634119_2.fastq.gz	Fastqsanger.gz
	SRR20634120_1.fastq.gz	Fastqsanger.gz
	SRR20634120_2.fastq.gz	Fastqsanger.gz
	SRR20634121_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance [exome-seq]

Project description:MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance [exome-seq]

| PRJNA862165 | ENA

MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance [RNA-seq]

Project description:MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance [RNA-seq]

| PRJNA862159 | ENA

MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance [exome-seq]

Project description:Pre-clinical model to study tumor immune resistance are essential. To this end, we generated cell lines from tumors induced on BrafV600E Pten-/- mice. The cell lines have been characterized to evaluate the tumor growth in vivo and response to immunotherapies. In addition, we have also chaacterised the DNA expression profile of the cell lines.

2023-07-30 | GSE209729 | GEO

MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance [RNA-seq]

2023-07-30 | GSE209725 | GEO

MeVa2.1.dOVA is a novel immune-refractory cell line to study tumor immune resistance

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

2023-07-30 | GSE209731 | GEO

Phase II Study of Immune Checkpoint Blockade with Pembrolizumab after High Dose Cytarabine in Relapsed/Refractory Acute Myeloid Leukemia

Project description:To address the role of immune dysregulation in AML, we conducted a phase II study of high-dose cytarabine followed by pembrolizumab 200 mg IV on day 14 to examine whether programmed death-1 inhibition improves clinical responses in relapsed/refractory (R/R) AML. Overall responders could receive pembrolizumab maintenance up to two years. Among thirty-seven patients enrolled, the overall response rate, composite complete remission rate (CRc; primary endpoint), and median overall survival (OS) were 46%, 38% and 11.1 months, respectively. Patients with refractory/early relapse and those receiving treatment as first salvage had encouraging outcomes (median OS 13.2 and 11.3 months, respectively). Grade >3 immune-related adverse events were rare (14%) and self-limiting. Patients who achieved CRc had a higher frequency of progenitor exhausted CD8+ T-cells in the bone marrow prior to treatment and a non-significant increase in baseline T-cell diversity.

2021-09-09 | GSE183415 | GEO

Immune Resistance Emerges from Tumor-Initiating Stem Cells

Project description:Tumors are initiated and maintained by a stem cell-like population. However, our bodies have a powerful immune surveillance system to clear out cancerous cells as they emerge. Whether tumor-initiating stem cells (tSCs) are programmed to resist anti-tumor immunity and/or how they overcome the barrier of immune surveillance remains poorly understood. To address these questions, we designed a murine skin tumor model that can be effectively challenged by adoptive cell transfer (ACT)-based immunotherapy. By lineage tracing the tumor cells that survive targeted T cell treatment, we discovered that a subset of TGFβ-responding tSCs are refractory and responsible for tumor relapse. Single cell RNA-sequencing revealed that during malignant transformation, these tSCs selectively acquire CD80. Thought to be an immune cell ligand, stem cell CD80 (scCD80) engagement with CTLA4 on activated cytotoxic T cells attenuates their attack. Moreover, without CD80 or in the face of CTLA4 blocking antibodies, tSCs become vulnerable to ACT immunotherapy. Our findings place the tumor-initiating stem cell at the crux of how immune checkpoint pathways are activated, and add a new mechanism to the fray.

2019-05-07 | GSE108679 | GEO

Refractory Cancer (RC) Program

Project description:Refractory Cancer (RC) Program

| PRJNA663002 | ENA

Refractory Cancer (RC) Program

Project description:Refractory Cancer (RC) Program

| PRJNA663003 | ENA

Reversal of pre-existing NGFR-driven tumor and immune therapy resistance

Project description:In spite of the remarkable clinical benefit from immune checkpoint blockade in melanoma, both intrinsic and acquired resistance prevent durable clinical responses in many patients. Whereas melanomas are known to acquire MART-1 T cell resistance by reversible phenotype switching to an NGFRhi state, less is known about mechanisms of intrinsic immune resistance. To mimic recurrent T cell attack, we chronically exposed a panel of (patient-derived) melanoma cell lines to clinically relevant MART-1 differentiation antigen-specific cytotoxic T cells. This led to strong enrichment of a pre-existing cell population that exhibited immune resistance in vitro and in mice. These fractions showed high expression of NGFR, were maintained stably, and were found to be present in patients’ melanomas prior to treatment. Remarkably, these NGFRhi melanoma cells also displayed resistance also to T cells recognizing antigens that are unrelated to melanoma differentiation. Furthermore, these cells exhibited multidrug-resistance to other therapies including BRAF + MEK inhibition, suggesting that they exist in a stable and distinct cellular state. Clinically corroborating these findings, a tumor-intrinsic NGFR signature predicted aPD-1 therapy resistance, while NGFRhi melanoma fractions in patients were associated with immune exclusion. Lastly, genetic or pharmacologic NGFR inhibition restored tumor sensitivity to T cell attack in vitro and in melanoma xenografts. These findings demonstrate the existence of a stable and pre-existing NGFRhi multitherapy-refractory melanoma subpopulation, which ought to be eliminated to revert intrinsic resistance to immunotherapeutic intervention.

2020-07-02 | GSE147091 | GEO

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