Microglial reprogramming: a potential new frontier in enhancing immunotherapy for melanoma brain metastasis

The brain is a common site of metastatic dissemination in advanced melanoma. Due to limited access to samples from human brain metastases, our understanding of the tumor microenvironment in the brain lags behind that of other sites, and murine studies are therefore highly informative. Rodriguez-Baena et al. conducted elegant studies of myeloid cells within melanoma brain metastases, demonstrating their plasticity and changes before and after colonization by melanoma cells. The immune-inhibitory changes in microglial cells may be reversed or mitigated by inhibition of RelA/NF-κB.

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Publication Details

Journal
Molecular Oncology
Published
2025-03-20
DOI
https://doi.org/10.1002/1878-0261.70028
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
Type
article
Field-Weighted Citation Impact
0.00
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article

Microglial reprogramming: a potential new frontier in enhancing immunotherapy for melanoma brain metastasis

Harriet M. Kluger, Noam Savion‐Gaiger, Dorin Bar‐Ziv
Molecular Oncology
Neuroinflammation and Neurodegeneration Mechanisms
article

Microglial reprogramming: a potential new frontier in enhancing immunotherapy for melanoma brain metastasis

Harriet M. Kluger, Noam Savion‐Gaiger, Dorin Bar‐Ziv
article en

Abstract

The brain is a common site of metastatic dissemination in advanced melanoma. Due to limited access to samples from human brain metastases, our understanding of the tumor microenvironment in the brain lags behind that of other sites, and murine studies are therefore highly informative. Rodriguez-Baena et al. conducted elegant studies of myeloid cells within melanoma brain metastases, demonstrating their plasticity and changes before and after colonization by melanoma cells. The immune-inhibitory changes in microglial cells may be reversed or mitigated by inhibition of RelA/NF-κB.

Molecular OncologyVol. 19(5)
Yale Cancer Center (US)
Good health and well-being
Openalex Percentile: Top 93%
Neuroinflammation and Neurodegeneration Mechanisms
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