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Mus musculus

ABSTRACT: ATR Mutations Promote the Growth of Melenama Tumor by Modulating the Immune Microenvironment [skin]

PROVIDER: PRJNA369213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5217290_1.fastq.gz	Fastqsanger.gz
	SRR5217290_2.fastq.gz	Fastqsanger.gz
	SRR5217291_1.fastq.gz	Fastqsanger.gz
	SRR5217291_2.fastq.gz	Fastqsanger.gz
	SRR5217292_1.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:ATR Mutations Promote the Growth of Melenama Tumor by Modulating the Immune Microenvironment [tumor]

| PRJNA369216 | ENA

ATR Mutations Promote the Growth of Melenama Tumor by Modulating the Immune Microenvironment

Project description:ATR Mutations Promote the Growth of Melenama Tumor by Modulating the Immune Microenvironment

| PRJNA369212 | ENA

ATR Mutations Promote the Growth of Melenama Tumor by Modulating the Immune Microenvironment [tumor]

Project description:Melanomas accumulate a high burden of mutations that could potentially generate neoantigens, yet these tumors are still able to suppress the immune response in order to facilitate their continued growth. In this study, we identify subsets of human melanoma tumors that have partial loss of function mutations in ATR, a kinase that recognizes and repairs UV-induced DNA damage and is required for cellular proliferation. ATR mutant tumors exhibit both the accumulation of multiple mutations and the altered expression of inflammatory genes, resulting in decreased T-cell recruitment and increased recruitment of macrophages known to spur tumor invasion. Taken together, these studies identify a novel mechanism by which melanoma cells modulate the immune microenvironment to allow continued tumor growth.

2017-01-31 | GSE94264 | GEO

ATR Mutations Promote the Growth of Melenama Tumor by Modulating the Immune Microenvironment [skin]

2017-01-31 | GSE94263 | GEO

Mus musculus

Project description:Entinostat decreases immune suppression to promote an anti-tumor response within a HER2+ breast tumor microenvironment.

| PRJNA683665 | ENA

Effect of Intravenous Infusion of Lidocaine on Patients Undergoing Radical Resection of Colorectal Tumors

Project description:Colorectal cancer (CRC) is one of the most common malignant tumors in the world. Surgical resection is the main treatment option for colorectal cancer patients. Surgery may enhance or accelerate tumor recurrence and metastasis. Multiple factors in the tumor microenvironment play important roles in tumor recurrence and metastasis, and modulating the tumor microenvironment can inhibit disease progression. Lidocaine has been found to inhibit tumor growth in animal experiments.

| 2743881 | ecrin-mdr-crc

Phenotyping tumor-immune microenvironment in vivo in skin cancer patients

Project description:Phenotyping tumor-immune microenvironment in vivo in skin cancer patients

| PRJNA750449 | ENA

TAZ facilitates breast tumor growth by promoting an immune-suppressive tumor microenvironment

Project description:TAZ facilitates breast tumor growth by promoting an immune-suppressive tumor microenvironment

| PRJNA1011907 | ENA

Mus musculus

Project description:Tumor immune microenvironment change after iRFA Raw sequence reads

| PRJNA1124610 | ENA

Intratumoral CpG-B promotes anti-tumoral neutrophil, cDC, and T cell cooperation without reprograming tolerogenic pDC

Project description:Cancer immunotherapies utilize distinct mechanisms to harness the power of the immune system to eradicate cancer cells. Therapeutic vaccines, aimed at inducing active immune responses against an existing cancer, are highly dependent on the immunological microenvironment, where many immune cell types display high levels of plasticity and, depending on the context, promote very different immunological outcomes. Among them, plasmacytoid dendritic cells (pDC), known to be highly immunogenic upon inflammation, are maintained in a tolerogenic state by the tumor microenvironment. Here we report that intratumoral (i.t.) injection of established solid tumors with CpG oligonucleotides-B (CpG-B) inhibits tumor growth. Interestingly, control of tumor growth was independent of tumor-associated (TA) pDC, which remained refractory to CpG-B stimulation and whose depletion did not alter the efficacy of the treatment. Instead, tumor growth inhibition subsequent to i.t. CpG-B injection depended on the recruitment of neutrophils into the milieu, resulting in the activation of conventional dendritic cells (cDC), subsequent increased anti-tumor T cell priming in draining lymph nodes, and enhanced effector T cell infiltration in the tumor microenvironment. These results reinforce the concept that intratumoral delivery of TLR9 agonists alters the tumor microenvironment by improving the anti-tumor activity of both innate and adaptive immune cells.

2018-03-23 | GSE112206 | GEO

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