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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ8)

ABSTRACT: Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ8)

PROVIDER: PRJNA578140 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10302412.fastq.gz	Fastqsanger.gz
	SRR10302413.fastq.gz	Fastqsanger.gz
	SRR10302414.fastq.gz	Fastqsanger.gz
	SRR10302415.fastq.gz	Fastqsanger.gz
	SRR10302416.fastq.gz	Fastqsanger.gz

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

Project description:Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ3)

Project description:Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ3)

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (scRNA-seq dataset: SZ11)

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (scRNA-seq dataset: SZ11)

Project description:In this study we searched for primary regulators of cancer-inhibitory inflammation using murine tumors of immune-dependent progressive or regressive fates linked to antagonistic inflammatory tumor microenvironments

2020-11-20 | GSE139046 | GEO

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ8)

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Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ3)

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Antagonistic Inflammatory Phenotypes Dictate Tumor Fate and Response to Immune Checkpoint Blockade.

Project description:Inflammation can support or restrain cancer progression and the response to therapy. Here, we searched for primary regulators of cancer-inhibitory inflammation through deep profiling of inflammatory tumor microenvironments (TMEs) linked to immune-dependent control in mice. We found that early intratumoral accumulation of interferon gamma (IFN-γ)-producing natural killer (NK) cells induced a profound remodeling of the TME and unleashed cytotoxic T cell (CTL)-mediated tumor eradication. Mechanistically, tumor-derived prostaglandin E2 (PGE2) acted selectively on EP2 and EP4 receptors on NK cells, hampered the TME switch, and enabled immune evasion. Analysis of patient datasets across human cancers revealed distinct inflammatory TME phenotypes resembling those associated with cancer immune control versus escape in mice. This allowed us to generate a gene-expression signature that integrated opposing inflammatory factors and predicted patient survival and response to immune checkpoint blockade. Our findings identify features of the tumor inflammatory milieu associated with immune control of cancer and establish a strategy to predict immunotherapy outcomes.

| S-EPMC7772804 | biostudies-literature

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

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

2020-11-20 | GSE139047 | GEO

Tumour mtDNA mutations drive aerobic glycolysis to enhance checkpoint blockade

Project description:Mitochondrial DNA (mtDNA) encodes essential machinery for respiration and metabolic homeostasis but is paradoxically among the most common targets of somatic mutations in the cancer genome, with truncating mutations in complex I genes being over-represented1 . While mtDNA mutations have been associated with both improved and worsened prognoses in several cancer lineages1–3, whether these mutations are drivers, or exert any functional effect on tumour biology remains controversial. Here we discover that complex I-encoding mtDNA mutations are sufficient to remodel the tumour immune landscape and therapeutic resistance to immune checkpoint blockade. Using mtDNA base editing technology we engineered recurrent truncating mutations in the mtDNA-encoded complex I gene, Mt-Nd5, into murine models of melanoma. Mechanistically, these mutations promoted utilisation of pyruvate as a terminal electron acceptor and increased glycolytic flux driven by an over-reduced NAD pool and NADH shuttling between GAPDH and MDH1, mediating a Warburg-like metabolic shift. In turn, without modifying tumour growth, this altered cancer cell-intrinsic metabolism reshaped the tumour microenvironment of mouse and human cancer in a mutation load-dependent fashion, encouraging an anti-tumour immune response. This subsequently sensitises both mouse and human cancers with high mtDNA mutant heteroplasmy to immune checkpoint blockade. Strikingly, patient lesions bearing >50% mtDNA mutation load demonstrated a >2.5-fold improved response rate to checkpoint inhibitor blockade. Taken together these data nominate mtDNA mutations as functional regulators of cancer metabolism and tumour biology, with potential for therapeutic exploitation and treatment stratification.

2023-11-08 | PXD039705 | Pride

Tumour mtDNA mutations drive aerobic glycolysis to enhance checkpoint blockade (part 2)

2023-11-08 | PXD044987 | Pride