The role of microglia and macrophages in glioma maintenance and progression

By D. Hambardzumyan, D. Gutmann, Helmut Kettenmann. Nature Neuroscience, 2015

1,502 citations recorded by the source corpus.

There is a growing recognition that gliomas are complex tumors composed of neoplastic and non-neoplastic cells, which each individually contribute to cancer formation, progression and response to treatment. The majority of the non-neoplastic cells are tumor-associated macrophages (TAMs), either of peripheral origin or representing brain-intrinsic microglia, that create a supportive stroma for neoplastic cell expansion and invasion. TAMs are recruited to the glioma environment, have immune functions, and can release a wide array of growth factors and cytokines in response to those factors produced by cancer cells. In this manner, TAMs facilitate tumor proliferation, survival and migration. Through such iterative interactions, a unique tumor ecosystem is established, which offers new opportunities for therapeutic targeting.

Subfields: Genetics, Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/18bf0defd73ae416ec876b47b93f44edfe5f5770

How researchers see this paper

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In Genetics

1. R. DePinho

In Immunology

1. A. Mantovani
2. M. Locati
3. G. Curtale
4. Guocan Wang
5. R. DePinho
6. A. Sica
7. P. Allavena
8. F. Martínez

In Neurology

1. A. Mantovani
2. R. DePinho
3. M. Locati

Citations in the corpus

• Diversity, Mechanisms and Significance of Macrophage Plasticity (2019, background): “As may have been expected on the basis of ontogeny (see above), microglia persisted in murine gliomas (115), resulting in the infiltration of macrophages of mixed origin.”
• Tumor evolution of glioma intrinsic gene expression subtype associates with immunological changes in the microenvironment (2017, background): “Tumor-associated macrophages, including either those of peripheral origin or representing brain-intrinsic microglia in glioma (Gabrusiewicz et al., 2016; Hambardzumyan et al., 2015), have been proposed as regulators of PN-to-MES transition through nuclear factor kB activation (Bhat et al.”