Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tumor cell-intrinsic Decr2 is necessary for immunotherapy efficacy

ABSTRACT: Tumor cell-intrinsic Decr2 is necessary for immunotherapy efficacy

PROVIDER: PRJEB75776 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR13110501.fastq.gz	Fastqsanger.gz
	ERR13110502.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Tumor cell-intrinsic Decr2 regulates ferroptosis and immunotherapy efficacy

Project description:Tumor cell-intrinsic Decr2 regulates ferroptosis and immunotherapy efficacy

| PRJNA1200063 | ENA

Targeting tumor-intrinsic S100A1 augments antitumor immunity and potentiates immunotherapy efficacy

Project description:Targeting tumor-intrinsic S100A1 augments antitumor immunity and potentiates immunotherapy efficacy

| PRJNA1205386 | ENA

Targeting tumor-intrinsic S100A1 augments antitumor immunity and potentiates immunotherapy efficacy

Project description:Immune checkpoint blockade (ICB) has revolutionized cancer treatment, but the therapeutic response is highly heterogeneous. A potential mode of resistance is tumor-intrinsic mechanisms leading to an immunosuppressive tumor microenvironment. However, the underlying interactive network remains elusive and the generalizable biomarkers and targeting strategies are still lacking. Here, we uncovered the potential of plasma S100 calcium-binding protein A1 (S100A1) in determining ICB efficacy based on liquid biopsy of patients with lung cancer. Muti-omics and functional studies suggested that tumor-intrinsic S100A1 expression correlates with an immunologically cold TME and resistance to ICB. Mechanistic investigations demonstrated that interfering with tumor-intrinsic S100A1/ubiquitin-specific protease 7/p65/granulocyte-macrophage colony-stimulating factor (GM-CSF) modulatory axis could potentiate an inflamed TME via promoting M1-like macrophage polarization and T cell function. GM-CSF priming was sufficient to enhance ICB response in tumors with high S100A1 expression. These findings defined S100A1 as a potential biomarker and a novel synergistic target for cancer immunotherapy.

2025-03-26 | GSE285657 | GEO

Tumor cell-intrinsic Decr2 regulates ferroptosis and immunotherapy efficacy

Project description:Increased or decreased B16 cell sensitivity to activated cytotoxic T lymphocytes.To identify tumor cell-intrinsic genes essential for antigen-specific CD8+ T cell killing, we utilized the B16.SIY melanoma cell line which expressed the model antigen SIY (SIYRYYGL) co-expressed with DsRed, that can be recognized by 2C CD8+ TCR transgenic (Tg) T cells. B16.SIY cells were transduced and selected to stably expressed a Cas9 gene, and then transduced with a genome-scale CRISPR gRNA library.Transduced cells were cultured for 8 days to provide time for gene disruption to occur, then were co-cultured with pre-activated 2C CD8+ T cells at a 2:1 Effector:Target ratio for 16 hours. By performing deep sequencing, we examined the sgRNA library representation in tumor cells with or without T cell co-incubation by MAGeCK analysis.

2025-06-30 | E-MTAB-13870 | biostudies-arrayexpress

Systematic identification of tumor-intrinsic resistance mechanisms and combinatorial therapy targets for immunotherapy

Project description:A number of reports have demonstrated that tumor-intrinsic mechanisms of resistance, such as the loss of genes critical for antigen presentation and inflammatory responses, along with the activation of various cellular signaling cascades, can limit the efficacy of immunotherapy. Strategies to sensitize tumor cells to immunotherapy may overcome some resistance mechanisms, but identifying therapeutic targets has remained challenging. Here, we integrate a two-cell type (2CT) whole-genome CRISPR-Cas9 screen with dynamic transcriptional profiling of the tumor/T cell interaction to comprehensively identify tumor genes that are induced to promote tumor survival. We assessed the therapeutic potential of pharmacological inhibition of these and other top CRISPR identified targets as combinatorial targets to improve the efficacy of tumor destruction by T cells.

2022-08-31 | GSE137824 | GEO

Explore tumor intrinsic factors regulating immunotherapy response in ovarian cancer

Project description:Despite approval of immunotherapy for the treatment of ovarian cancer patients, the majority of patients fail to respond to immunotherapy or relapse following initial response. These failures may be attributed to immunosuppressive mechanisms co-opted by tumor cells. However, it is challenging to use conventional methods to systematically evaluate the potential of tumor intrinsic factors to act as immune regulators in patients with cancer. To identify immunosuppressive mechanisms in non-responders to cancer immunotherapy in ovarian cancer , we firstly performed an unbiased genome-wide CRISPR immune screens to explore tumor intrinsic factors which regulates ovarian cancer cell lines response to T cell mediated killing. Then we integrated the in vitro CRISPR screen results with multi-omics clinical data to generate a sub-library including top candidates for in vivo CRISPR screen to further evaluate the role of potential tumor intrinsic factors in regulating ovarian cancer cell response to immunotherapy with using the immune checkpoint blocker. Collectively, the data provide a rich resource of novel targets for rational immuno-oncology combinations.

2025-12-17 | GSE267517 | GEO

Tumor-intrinsic ST3GAL3 Activity Blunts Anti-tumor Immune and Drives Immunotherapy Resistance

Project description:Tumor-intrinsic ST3GAL3 Activity Blunts Anti-tumor Immune and Drives Immunotherapy Resistance

| PRJNA879768 | ENA

Explore tumor intrinsic factors regulating immunotherapy response in ovarian cancer

Project description:Explore tumor intrinsic factors regulating immunotherapy response in ovarian cancer

| PRJNA1111761 | ENA

Glioma-intrinsic MAPK/ERK signaling promotes immunotherapy efficacy through T cell infiltration and interferon responses

Project description:Glioblastoma (GBM) remains a formidable challenge in neuro-oncology, with immune checkpoint blockade (ICB) only showing efficacy in some patients, while the mechanisms governing therapeutic responsiveness are poorly defined. Although MAPK/ERK signaling correlates with survival following ICB, its causal role and mechanisms underlying tumor immunogenicity remain unclear. Here, we perform in vivo kinome-wide CRISPR/Cas9 screens in murine gliomas where we identify RAF-MEK-ERK axis as the strongest modulators of glioma susceptibility to anti-programmed cell death protein 1 (anti-PD-1) therapy and CD8+ T cell recognition. Experimentally-induced ERK phosphorylation (p-ERK) enhances survival after anti-PD-1 and anti-CLTA4, leading to durable antitumor immunity upon rechallenge. Additionally, glioma cell p-ERK promotes increased interferon responses and T cell infiltration. Notably, BRAF/MEK inhibition disrupts interferon programs and tumor-microglia interactions in BRAFV600E ex vivo in human GBM/brain slice cultures. Our findings elucidate that tumor-intrinsic MAPK/ERK promotes immunotherapy response, interferon responses, T cell tumor infiltration, and GBM cell-microglia interactions.

2026-05-21 | GSE331374 | GEO

Targeting tumor-intrinsic SLC16A3 to enhance anti-PD-1 efficacy via tumor immune microenvironment reprogramming

Project description:Targeting tumor-intrinsic SLC16A3 to enhance anti-PD-1 efficacy via tumor immune microenvironment reprogramming

| PRJNA978069 | ENA