Together, these data support a clinical trial designed to target PD-L1 with avelumab and haNK cells, potentially offering a novel immunotherapeutic approach for patients with malignant meningioma.
While several studies have examined p53 both at the level of the gene and the protein in both benign and malignant meningiomas, its role remains controversial, particularly with regard to the discrepancy between p53 over-expression and gene mutation.
The higher the p53 protein expression rate, the poorer the histologic grade (9.5%, 72.7%, and 88.9% in benign, atypical and malignant meningioma, respectively) (p=0.000).
Deletion of the p16(INK4a)/p14(ARF) locus is found in both benign and malignant meningiomas, while mutation of the p53 tumor suppressor gene is uncommon.
RNA interference-mediated targeting of urokinase plasminogen activator receptor and matrix metalloproteinase-9 gene expression in the IOMM-lee malignant meningioma cell line inhibits tumor growth, tumor cell invasion and angiogenesis.
Our study revealed that abrogation of cathepsin B and MMP-9 expression decreased the activation of major proteins involved in MAP kinase and PI3 kinase pathways indicating that targeting these proteases may hinder intracellular signaling and thus decrease cell survival and proliferation in malignant meningiomas.
Most importantly, p16 deletion was strongly associated with survival in the anaplastic meningioma cohort, with a risk ratio for death of 6.79 (p = 0.016).
Bioinformatics analysis and mechanism experiments demonstrated that LINC00702 acted as the molecular sponge of miR-4652-3p to upregulate ZEB1 in malignant meningioma.