An official website of the United States government
The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before
sharing sensitive information, make sure you’re on a federal
government site.
The site is secure.
The https:// ensures that you are connecting to the
official website and that any information you provide is encrypted
and transmitted securely.
1 Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: sourav.ghosh@yale.edu.
2 Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: carla.rothlin@yale.edu.
1 Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: sourav.ghosh@yale.edu.
2 Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: carla.rothlin@yale.edu.
Kloosterman and colleagues studied molecular and cellular changes during radiation therapy and disease recurrence across molecular subtypes of glioblastoma. They uncovered a distinct immune-cancer cell metabolic crosstalk during proneural/oligodendrocyte progenitor cell-like to mesenchymal-like transition, wherein macrophages feed on cholesterol-rich myelin debris to provide lipids to mesenchymal tumor cells, thereby fueling glioblastoma growth.
Declaration of interests C.V.R. is a member of the Trends in Immunology Advisory Board.
Figures
Figure 1.. Macrophage-tumor metabolic crosstalk in mesenchymal…
Figure 1.. Macrophage-tumor metabolic crosstalk in mesenchymal glioblastoma.
The schematic represents the model proposed by…
Figure 1.. Macrophage-tumor metabolic crosstalk in mesenchymal glioblastoma.
The schematic represents the model proposed by Kloosterman and colleagues [6], where tumor-associated macrophages phagocytose myelin debris to become “lipid-laden”, acquiring a unique transcriptional state in which lipids are transferred to mesenchymal tumor cells, leadinf to tumor cell proliferation and glioblastoma growth. Complementing this interaction, the high glycolytic state of mesenchymal cancer cells supports the induction of the “lipid laden” state of the macrophages [6].
Johnson BE et al. (2014) Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma. Science 343, 189–193. 10.1126/science.1239947
-
DOI
-
PMC
-
PubMed
Kim H. et al. (2015) Whole-genome and multisector exome sequencing of primary and post-treatment glioblastoma reveals patterns of tumor evolution. Genome Res 25, 316–327. 10.1101/gr.180612.114
-
DOI
-
PMC
-
PubMed
Wang J. et al. (2016) Clonal evolution of glioblastoma under therapy. Nat Genet 48, 768–776. 10.1038/ng.3590
-
DOI
-
PMC
-
PubMed
Morantz RA et al. (1979) Macrophages in experimental and human brain tumors. Part 1: Studies of the macrophage content of experimental rat brain tumors of varying immunogenicity. J Neurosurg 50, 298–304. 10.3171/jns.1979.50.3.0298
-
DOI
-
PubMed
Morantz RA et al. (1979) Macrophages in experimental and human brain tumors. Part 2: studies of the macrophage content of human brain tumors. J Neurosurg 50, 305–311. 10.3171/jns.1979.50.3.0305
-
DOI
-
PubMed