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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche

ABSTRACT: Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche

PROVIDER: PRJNA816518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18333307.fastq.gz	Fastqsanger.gz
	SRR18333308.fastq.gz	Fastqsanger.gz
	SRR18333309.fastq.gz	Fastqsanger.gz
	SRR18333310.fastq.gz	Fastqsanger.gz
	SRR18333311.fastq.gz	Fastqsanger.gz

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (PADMEseq)

Project description:Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (PADMEseq)

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (PADMEseq)

Project description:Immunotherapy is a promising treatment for Triple-Negative Breast Cancer (TNBC), but patients recur, arising the need to understand mechanisms of resistance. We discovered that in primary breast cancer, tumor cells that survive T-cell attack are in a quiescent state. Quiescent Cancer Cells (QCCs) are found clustering together forming regions with reduced immune infiltration. QCCs display superior tumorigenic capacity and higher expression of stemness genes than their proliferative counterparts. We adapted single-cell-RNA-sequencing with precise spatial resolution to profile infiltrating cells inside and outside QCC niches. This transcriptomic analysis revealed hypoxia-induced programs and identified more exhausted T-cells, tumor-protective fibroblasts, and dysfunctional dendritic cells inside clusters of QCCs. This uncovered differential phenotypes in infiltrating cells based on their specific intra-tumor location. Thus, QCCs constitute immunotherapy-resistant reservoirs by orchestrating a local hypoxic immune-suppressive milieu that blocks T-cell function. Eliminating QCCs holds the promise to counteract resistance to immunotherapy and prevent disease recurrence in TNBC.

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (QCC vs proliferative cells from tumors Bulk RNA)

Project description:Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (QCC vs proliferative cells from tumors Bulk RNA)

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (QCC vs proliferative cells from tumors Bulk RNA)

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (GFP:mCherry 1:1 4T07 mix tumors after Jedi killing Bulk RNA)

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (GFP:mCherry 1:1 4T07 mix tumors after Jedi killing Bulk RNA)

Project description:Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche (GFP:mCherry 1:1 4T07 mix tumors after Jedi killing Bulk RNA)

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Quiescent cancer cells resist T cell attack by forming an immunosuppressive niche

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

2022-04-20 | GSE198715 | GEO

Tumor-infiltrating Monocytic Myeloid-derived suppressor cells play a key role in forming immunosuppressive microenvironment in human gastric cancer

Project description:The present data suggest that M-MDSC, play a predominant role in forming the immunosuppressive microenvironment in GC.

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A combinatorial attack strategy uncovers a molecular rationale for treating inflammatory cardiomyopathy

Project description:Here we show how the cardiac transcriptome evolves during murine myocarditis revealing early and persistent activation of cytokine and chemokine-signalling pathways together with innate immune, antigen-presentation, complement and cell-adhesion pathway activation. We identified a 50-gene subnetwork based on expression importance and quantified network tolerance to combinatorial node removal to determine target-specific therapeutic potential. Combinatorial attack of Traf2, Nfkb1, Rac1 and Vav1 causes 80% subnetwork disconnection. NFKB1 and RAC1 are targeted by prednisolone and azathioprine, creating 56% network disconnection, establishing a molecular rationale for immunosuppressive therapy. Additional combinatorial attack of BTK and PIK3CD with approved therapeutics causes 72% network disconnection, suggesting that they could be re-purposed to treat inflammatory cardiomyopathy. We propose that the combinatorial attack strategy developed here could be applied to other immune-mediated diseases.

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short and long attack latency mice

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