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Microglial reprogramming enhances anti-tumor immunity and immunotherapy response in melanoma brain metastases.

ABSTRACT: Microglial reprogramming enhances anti-tumor immunity and immunotherapy response in melanoma brain metastases.

PROVIDER: PRJNA1098587 | ENA |

REPOSITORIES: ENA

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Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

| PRJNA1205401 | ENA

Microglial reprogramming enhances anti-tumor immunity and immunotherapy response in melanoma brain metastases [RNA-seq]

Project description:Microglial reprogramming enhances anti-tumor immunity and immunotherapy response in melanoma brain metastases [RNA-seq]

| PRJNA1098589 | ENA

Microglial reprogramming enhances antitumor immunity and immunotherapy response in melanoma brain metastases

Project description:Melanoma is one of the tumor types with the highest risk of brain metastasis. However, the biology of melanoma brain metastasis and the contribution of the brain immune microenvironment to the responses to therapies remain insufficiently characterized. By using preclinical models and single-cell transcriptomics, we identify a mechanism to promote antitumor immunity in melanoma brain metastasis. We show that activation of the Rela/NF-kB pathway in microglia promotes melanoma brain metastasis and that targeting this pathway elicits microglia reprogramming towards a proinflammatory phenotype that enhances antitumor immunity and reduces brain metastatic burden. Additionally, proinflammatory microglial markers in melanoma brain metastasis correlate with better responses to immune checkpoint inhibitors in patients and we show that Rela/NF-kB targeting improves responses to these therapies in the brain. Thus, we propose targeting Rela/NF-kB in activated microglia as a strategy to promote antitumor immunity and responses to immune checkpoint inhibitors in melanoma brain metastasis.

2025-02-07 | GSE285670 | GEO

Microglial reprogramming enhances anti-tumor immunity and immunotherapy response in melanoma brain metastases [RNA-seq]

Project description:Melanoma is one of the solid tumor types with the highest risk of brain metastasis. However, the biology of melanoma brain metastasis and the contribution of the brain immune microenvironment to the responses to therapies remain insufficiently characterized. By using preclinical models and single-cell transcriptomics, we identify microglia, as critical regulators of melanoma biology in the brain. We show that activation of the Rela/NF-kB pathway in microglia promotes melanoma brain metastasis and that targeting this pathway elicits microglia reprogramming towards a pro-inflammatory phenotype that enhances anti-tumor immunity and reduces brain metastatic burden. Additionally, canonical and pro-inflammatory microglial markers in melanoma brain metastasis correlate with better responses to immune checkpoint inhibitors in patients and we show that Rela/NF-kB targeting improves responses to these therapies in the brain. Thus, we propose targeting Rela/NF-kB in activated microglia as a strategy to promote anti-tumor immunity and to improve the response to immune checkpoint inhibitors in melanoma brain metastasis.

2025-02-07 | GSE263622 | GEO

Microglial reprogramming enhances anti-tumor immunity and immunotherapy response in melanoma brain metastases.

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

2025-02-06 | GSE263625 | GEO

Progressing vs regressing melanoma metastases

Project description:We documented the transcriptional pattern of 3 progressing and 2 regressing synchronous melanoma metastases from the same patient following M-VAX treatment. Two-condition experiment, Progressing vs regressing metastases. 3 progressing and 2 regressing metastases extracted from the same patient after M-VAX immunotherapy. One replicate per array.

2010-09-11 | E-GEOD-24067 | biostudies-arrayexpress

Microglial reprogramming by targeting NF-kB enhances anti-tumor immunity and responses to immunotherapy in melanoma brain metastasis [scRNAseq_Nras-MBM]

2025-02-07 | GSE263623 | GEO

Microglial reprogramming by targeting NF-kB enhances anti-tumor immunity and responses to immunotherapy in melanoma brain metastasis [scRNAseq_Nras-MBM]

Project description:Microglial reprogramming by targeting NF-kB enhances anti-tumor immunity and responses to immunotherapy in melanoma brain metastasis [scRNAseq_Nras-MBM]

| PRJNA1098591 | ENA

Targeting the HSP47-Collagen Axis Inhibits Brain Metastasis by Reversing M2 Microglial Polarization and Restoring Anti-Tumor Immunity

Project description:Brain metastases (BrMs) are the leading cause of death in patients with solid cancers. BrMs exhibit a highly immunosuppressive milieu and poor response to immunotherapies; however, the underlying mechanism remains largely unclear. Here, we show that upregulation of HSP47 in tumor cells drives metastatic colonization and outgrowth in brain by creating an immunosuppressive microenvironment. HSP47-mediated collagen deposition in the metastatic niche promotes microglial polarization to M2 phenotype via the α2β1 integrin/NF-κB pathway, which upregulates the anti-inflammatory cytokines and represses CD8+ T cell anti-tumor responses. Depletion of microglia reverses HSP47-induced inactivation of CD8+ T cells and abolishes brain metastasis. Col003, an inhibitor disrupting HSP47-collagen association restores an anti-tumor immunity and enhances the efficacy of anti-PD-L1 immunotherapy in BrMs-bearing mice. Our study supports that HSP47 is a critical determinant of M2 microglial polarization and immunosuppression, and blocking the HSP47-collagen axis represents a promising therapeutic strategy against brain metastatic tumors.

2024-03-22 | GSE261941 | GEO

Neoadjuvant chemotherapy modulates T cell responses in high-grade serous ovarian cancer metastases

Project description:Our data suggest that neoadjuvant chemotherapy enhances anti-cancer responses of T cells in peritoneal metastases of patients with high-grade serous ovarian cancer but does not decrease levels of immune checkpoint molecules, providing a rationale for sequential chemo-immunotherapy. tRNA was isolated from 35 omental tissue samples of HGSOC metastases either pre or post NACT treatment. RNASeq was performed on poly-A selected mRNA fragments, 100 b.p paired end, and strand specific, on average 40 million reads per sample.

2016-07-27 | E-GEOD-71340 | biostudies-arrayexpress

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