Both YAP1-MAML2 and constitutively active YAP1 drive the formation of tumors that resemble NF2 mutant meningiomas in mice [mouse]

We analyzed the expression profiles of human and mouse meningiomas (driven by NF2 loss, YAP1-MAML2, TRAF7/KLF4/SMO1/AKT1, or constitutively active non-fusion YAP1). We found that YAP1-MAML2 meningiomas resemble NF2mutant tumors and constitutively exert de-regulated YAP1 activity that is dependent on the interaction with TEADs. Gene expression data from mouse RCAS-YAP1-MAML2-v2 or RCAS-NLS-2SA-YAP1-derived meningioma-like tumors (either extra-cranial, extra-axial, or intra-ventricular tumors).