Meningioma–Brain Crosstalk: A Scoping Review

SIMPLE SUMMARY: Meningioma is the most common primary intracranial tumour. However, the histopathological diagnosis remains simplistic and to some extent insufficient compared to other brain tumours. Surgery is the primary treatment, and radiation therapy is secondary treatment for tumours that recur. Traditional chemotherapy has so far been ineffective, as these tumours are resistant, and research on meningioma biology is lacking compared to other tumour types. The tumoral microenvironment (TME) plays a key role in understanding various cancers. In meningiomas, however, the TME is poorly understood. It is unknown how the brain immune cells contribute to meningioma behaviour and aggressiveness, and the relationship between meningioma cells and TME involved in treatment resistance also needs to be investigated. It is therefore necessary to explore if the literature holds any evidence regarding meningioma–brain crosstalk in order to identify the gaps of knowledge. The sparse amount of available literature on the subject necessitates a scoping review approach. ABSTRACT: Background: In recent years, it has become evident that the tumoral microenvironment (TME) plays a key role in the pathogenesis of various cancers. In meningiomas, however, the TME is poorly understood, and it is unknown if glia cells contribute to meningioma growth and behaviour. Objective: This scoping review investigates if the literature describes and substantiates tumour–brain crosstalk in meningiomas and summarises the current evidence regarding the role of the brain parenchyma in the pathogenesis of meningiomas. Methods: We identified studies through the electronic database PubMed. Articles describing glia cells and cytokines/chemokines in meningiomas were selected and reviewed. Results: Monocytes were detected as the most abundant infiltrating immune cells in meningiomas. Only brain-invasive meningiomas elicited a monocytic response at the tumour–brain interface. The expression of cytokines/chemokines in meningiomas has been studied to some extent, and some of them form autocrine loops in the tumour cells. Paracrine interactions between tumour cells and glia cells have not been explored. Conclusion: It is unknown to what extent meningiomas elicit an immune response in the brain parenchyma. We speculate that tumour–brain crosstalk might only be relevant in cases of invasive meningiomas that disrupt the pial–glial basement membrane.