Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acquired immunotherapy resistance in PDA (ATAC-seq)

ABSTRACT: Acquired immunotherapy resistance in PDA (ATAC-seq)

PROVIDER: PRJNA918632 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22987380_1.fastq.gz	Fastqsanger.gz
	SRR22987380_2.fastq.gz	Fastqsanger.gz
	SRR22987381_1.fastq.gz	Fastqsanger.gz
	SRR22987381_2.fastq.gz	Fastqsanger.gz
	SRR22987382_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Acquired immunotherapy resistance in PDA

Project description:Acquired immunotherapy resistance in PDA

| PRJNA918626 | ENA

Acquired immunotherapy resistance in PDA (RNA-seq)

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

| PRJNA918633 | ENA

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

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

| PRJNA1046562 | ENA

Clinical and molecular features of acquired resistance to immunotherapy [ATAC-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 | GSE249001 | GEO

Cancer cell self-built physical barriers promote acquired resistance to immunotherapy [spatial]

Project description:Drug resistance is the principal challenge of cancer therapies, including recently developed immunotherapy. More and more popular use of immunotherapy, especially treatments with immune checkpoint inhibitors (ICIs), witnesses explosively increasing cases of both primary and acquired immunotherapy resistance. While primary resistance has been extensively studied, mechanisms underlying acquired resistance of immunotherapy are less understood. Here we reported that tumor cells could develop acquired resistance to ICI treatment through self-built collagen-containing physical barriers in non-small cell lung cancer (NSCLC). We found that tumor cells expressed high levels of multiple collagen genes, including COL3A1 and COL6A1, and were fully covered with collagen fibers. COL3A1 formed a castle-like structure of a cluster of tumor cells and prevented the infiltration of T cells, while COL6A1 seemed to be an armor-like structure of each tumor cell and protected them from attack by cytotoxic T cells. Genetic or pharmaceutic disruption of these collagens, by warfarin, a commonly used medicine, significantly reversed the acquired resistance. Thus, our data reveal an unprecedented tumor cell-intrinsic mechanism, mediated by collagen-containing physical barriers, of acquired immunotherapy resistance, which immediately suggests a treatment option for patients.

2025-02-01 | GSE261890 | GEO