Project description
Surgical resection is the primary treatment for meningiomas, but radiotherapy (RT) is commonly used as first-line therapy in cases of incomplete resection, difficult tumour locations, or recurrence, especially since effective chemotherapy options are lacking. RT influences cytokine levels within the tumour microenvironment (TME), affecting immune cell signalling in ways that can either promote or inhibit tumour growth. While several clinical and preclinical trials have explored radioimmunotherapy, success has been limited. No immunotherapy for meningiomas has yet gained FDA approval, though early-phase trials targeting IFN-alpha and PD-1 have been conducted.
Emerging evidence highlights the crucial role of the immune TME, particularly macrophages, in meningioma progression and therapy resistance. Our previous study showed that recurrent meningiomas have elevated IL-6 expression, which further increased when meningioma spheroids were co-cultured with M2-polarised macrophages.
The impact of RT on cytokine signalling in this context remains unclear, as does how immune regulation contributes to treatment resistance or tumour progression. This represents a significant gap in scientific and clinical understanding.
Building on these findings, we hypothesise that RT modulates secretion of both pro-tumoral (e.g., IL-6, IL-10, TGF-beta) and anti-tumoral (e.g., IFN-gamma, TNF-alpha) cytokines within the TME under co-culture conditions. We plan to use a flow-based multiplex assay to profile cytokine changes post-RT, identifying those most significantly altered to better understand and potentially target immune interactions in meningioma.
