Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acquired resistance to targeted therapy confers cross-resistance to immunotherapy

ABSTRACT: Acquired resistance to targeted therapy confers cross-resistance to immunotherapy

PROVIDER: PRJNA548090 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11504802.fastq.gz	Fastqsanger.gz
	SRR11504803.fastq.gz	Fastqsanger.gz
	SRR11504804.fastq.gz	Fastqsanger.gz
	SRR11504805.fastq.gz	Fastqsanger.gz
	SRR11504806.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 242

Similar Datasets

Acquired immunotherapy resistance in PDA

Project description:Acquired immunotherapy resistance in PDA

| PRJNA918626 | ENA

Acquired resistance to targeted therapy confers cross-resistance to immunotherapy

Project description:We identify a profoundly remodelled TME in targeted therapy resistant (RTT) tumours. We provide bulk transcriptomic data of targeted therapy naive (NTT) and RTT tumours of 3 murine models. Additionally, we provide low-input sequencing of CD103+ dendritic cells and T cells from NTT and RTT Braf/Pten tumours. We identified that in RTT cell lines the MAPK pathway is reactivated and provide SLAM-seq data to determine transcriptional targets of MAPK pathway inhibition in NTT and RTT cell lines. We also provide ATAC-Seq data of NTT and RTT cell lines sorted from tumors of the Braf/Pten melanoma model.

2021-06-26 | GSE132443 | GEO

Acquired immunotherapy resistance in PDA (RNA-seq)

Project description:Acquired immunotherapy resistance in PDA (RNA-seq)

| PRJNA918633 | ENA

Acquired immunotherapy resistance in PDA (ATAC-seq)

Project description:Acquired immunotherapy resistance in PDA (ATAC-seq)

| PRJNA918632 | ENA

Clinical and molecular features of acquired resistance to immunotherapy [RNA-seq]

Project description:Although immunotherapy with PD-(L)1 blockade is routine for lung cancer, little is known about acquired resistance. Among 1,201 patients with non-small cell lung cancer (NSCLC) treated with PD-(L)1 blockade, acquired resistance is common, occurring in >60% of initial responders. Acquired resistance shows differential expression of inflammation and interferon (IFN) signaling. Relapsed tumors can be separated by upregulated or stable expression of IFNγ response genes. Upregulation of IFNγ response genes is associated with putative routes of resistance characterized by signatures of persistent IFN signaling, immune dysfunction, and mutations in antigen presentation genes which can be recapitulated in multiple murine models of acquired resistance to PD-(L)1 blockade after in vitro IFNγ treatment. Acquired resistance to PD-(L)1 blockade in NSCLC is associated with an ongoing, but altered IFN response. The persistently inflamed, rather than excluded or deserted, tumor microenvironment of acquired resistance informs therapeutic strategies to effectively reprogram and reverse acquired resistance.

2024-01-11 | GSE249000 | GEO

Clinical and molecular features of acquired resistance to immunotherapy [ATAC-seq]

2024-01-11 | GSE249001 | GEO

scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [1]

Project description:Serial blood draws from a single patient and serial tumor biopsies from the same patient with metastatic Merkel cell polyomavirus Merkel cell carcinoma, who was treated with cellular immunotherapy targeting MCPyV (autologous endogenous T cell therapy) followed by checkpoint inhibitors (anti-PD1 and anti-CTLA4). The patient had a 22 month clinical response followed by late/acquired resistance. We performed scRNAseq using the 10x genomics 3' Chromium expression assay to determine potential mechanisms contributing to immunotherapy response and late resistance

2018-09-01 | GSE117988 | GEO

Clinical and molecular features of acquired resistance to immunotherapy in non-small cell lung cancer

2024-01-11 | GSE248249 | GEO

Clinical and molecular features of acquired resistance to immunotherapy in non-small cell lung cancer

Project description:Although cancer immunotherapy with PD-(L)1 blockade is now routine treatment for patients with lung cancer, remarkably little is known about acquired resistance. We examined 1,201 patients with NSCLC treated with PD-(L)1 blockade to clinically characterize acquired resistance, finding it to be common (occurring in more than 60% of initial responders), with persistent but diminishing risk over time, and with distinct metastatic and survival patterns compared to primary resistance. To examine the molecular phenotype and potential mechanisms of acquired resistance, we performed whole transcriptome and exome tumor profiling in a subset of NSCLC patients (n=29) with acquired resistance. Systematic immunogenomic analysis revealed that tumors with acquired resistance differentially expressed features of inflammation and interferon (IFN) signalling. In particular, relapsed tumors could be separated into those with either upregulated or with stable expression of IFNγ response genes. Tumors with upregulated IFNγ response genes were associated with putative routes of resistance characterized by signatures of persistent IFN signaling, immune dysfunction, and mutations in antigen presentation genes. Transcriptomic profiling of cancer cells from multiple murine models of acquired resistance to PD-(L)1 blockade also showed evidence of high IFN-stimulated genes coupled to an altered or attenuated induced response after in vitro IFNγ treatment. In summary, we characterized clinical and molecular features of acquired resistance to PD-(L)1 blockade in NSCLC and found evidence of ongoing but altered IFN response. The persistently inflamed, rather than excluded or deserted, tumor microenvironment of acquired resistance informs therapeutic strategies to effectively reprogram and reverse acquired resistance.

2024-01-01 | GSE246922 | GEO

scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [2]

Project description:scRNAseq reveals mechanisms of Merkel cell carcinoma acquired immunotherapy resistance [2]

| PRJNA484204 | ENA