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Nat Rev Neurol. 2018 Aug;14(8):482-495. doi: 10.1038/s41582-018-0025-8.

Multidimensional communication in the microenvirons of glioblastoma.

Author information

1
Department of Neurology and Center for Molecular Imaging Research, Department of Radiology, Massachusetts General Hospital and Program in Neuroscience, Harvard Medical School, Boston, MA, USA. M.L.D.Broekman-16@umcutrecht.nl.
2
Department of Neurosurgery, Brain Center Rudolf Magnus, Institute of Neurosciences, University Medical Center, Heidelberglaan, Utrecht, Netherlands. M.L.D.Broekman-16@umcutrecht.nl.
3
Department of Neurology and Center for Molecular Imaging Research, Department of Radiology, Massachusetts General Hospital and Program in Neuroscience, Harvard Medical School, Boston, MA, USA.
4
Department of Neurosurgery, Brain Center Rudolf Magnus, Institute of Neurosciences, University Medical Center, Heidelberglaan, Utrecht, Netherlands.
5
The Center for Immunology and Inflammatory Diseases and Department of Medicine, Massachusetts General Hospital, Charlestown, MA, USA.
6
Program in Immunology, Harvard Medical School, Boston, MA, USA.
7
Department of Neurology, Ann Romney Center for Neurologic Diseases, Initiative for RNA Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
8
Department of Neurology and Center for Molecular Imaging Research, Department of Radiology, Massachusetts General Hospital and Program in Neuroscience, Harvard Medical School, Boston, MA, USA. breakefield@hms.harvard.edu.

Abstract

Glioblastomas are heterogeneous and invariably lethal tumours. They are characterized by genetic and epigenetic variations among tumour cells, which makes the development of therapies that eradicate all tumour cells challenging and currently impossible. An important component of glioblastoma growth is communication with and manipulation of other cells in the brain environs, which supports tumour progression and resistance to therapy. Glioblastoma cells recruit innate immune cells and change their phenotype to support tumour growth. Tumour cells also suppress adaptive immune responses, and our increasing understanding of how T cells access the brain and how the tumour thwarts the immune response offers new strategies for mobilizing an antitumour response. Tumours also subvert normal brain cells - including endothelial cells, neurons and astrocytes - to create a microenviron that favours tumour success. Overall, after glioblastoma-induced phenotypic modifications, normal cells cooperate with tumour cells to promote tumour proliferation, invasion of the brain, immune suppression and angiogenesis. This glioblastoma takeover of the brain involves multiple modes of communication, including soluble factors such as chemokines and cytokines, direct cell-cell contact, extracellular vesicles (including exosomes and microvesicles) and connecting nanotubes and microtubes. Understanding these multidimensional communications between the tumour and the cells in its environs could open new avenues for therapy.

PMID:
29985475
DOI:
10.1038/s41582-018-0025-8

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