Meningiomas are thought to arise from the meningeal coverings of the brain and the spinal cord. They are classified into three WHO grades and 15 histological subtypes. Nearly 80% of meningiomas are benign, corresponding to WHO grade I, such as meningothelial and fibroblastic subtypes, while the remaining 20% are malignant, belonging to WHO grade II (such as atypical subtypes) and WHO grade III (such as anaplastic subtypes). A small portion of benign meningiomas may recur after surgery, and even progress into malignant meningiomas. Malignant meningiomas are characterized by aggressive growth, high mitotic figures, preferred invasion into surrounding tissues, recurrence after surgical resection, and short disease-specific survival. The clinical outcome strongly depends on the WHO grade: patients with benign meningiomas have five-year survival rates of 92%. 5-year survival decreases in atypical meningiomas to 78%, and in patients with WHO III meningiomas survival rates drop down to 47%. Thus, effective treatment for malignant meningiomas is still difficult. Recent studies revealed several genetic alterations in meningiomas including NF2, TRAF7, AKT1, SMO, KLF4, POLR2A, PIK3CA, and TERT promoter mutations. The identification of these mutations has led to the investigation of inhibitors targeting proteins such as AKT1, SMO, mTOR, and FAK. Several clinical trials investigating meningioma treatment are currently underway (NCT02523014; NCT03071874; NCT02831257; EORTC-1320).
This Research Topic will discuss the recent advances in meningioma research. Original research or Review articles focusing on genetics, molecular oncology, imaging, surgery, or pathology are welcome. Topics include but are not limited to:
1) Current trends or concerns on genetic mutations in meningioma;
2) Meningioma cell line or meningioma stem cells in situ studies;
3) Signaling pathways relative to meningioma pathogenesis;
4) Biomarkers or molecular targets for meningioma diagnosis and therapy;
5) Imaging techniques used for meningioma preoperative differentiation and intraoperative monitoring;
6) Surgical intervention for meningioma.
7) Modeling meningioma: patient-derived xenografts and genetically engineered mouse models.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Meningiomas are thought to arise from the meningeal coverings of the brain and the spinal cord. They are classified into three WHO grades and 15 histological subtypes. Nearly 80% of meningiomas are benign, corresponding to WHO grade I, such as meningothelial and fibroblastic subtypes, while the remaining 20% are malignant, belonging to WHO grade II (such as atypical subtypes) and WHO grade III (such as anaplastic subtypes). A small portion of benign meningiomas may recur after surgery, and even progress into malignant meningiomas. Malignant meningiomas are characterized by aggressive growth, high mitotic figures, preferred invasion into surrounding tissues, recurrence after surgical resection, and short disease-specific survival. The clinical outcome strongly depends on the WHO grade: patients with benign meningiomas have five-year survival rates of 92%. 5-year survival decreases in atypical meningiomas to 78%, and in patients with WHO III meningiomas survival rates drop down to 47%. Thus, effective treatment for malignant meningiomas is still difficult. Recent studies revealed several genetic alterations in meningiomas including NF2, TRAF7, AKT1, SMO, KLF4, POLR2A, PIK3CA, and TERT promoter mutations. The identification of these mutations has led to the investigation of inhibitors targeting proteins such as AKT1, SMO, mTOR, and FAK. Several clinical trials investigating meningioma treatment are currently underway (NCT02523014; NCT03071874; NCT02831257; EORTC-1320).
This Research Topic will discuss the recent advances in meningioma research. Original research or Review articles focusing on genetics, molecular oncology, imaging, surgery, or pathology are welcome. Topics include but are not limited to:
1) Current trends or concerns on genetic mutations in meningioma;
2) Meningioma cell line or meningioma stem cells in situ studies;
3) Signaling pathways relative to meningioma pathogenesis;
4) Biomarkers or molecular targets for meningioma diagnosis and therapy;
5) Imaging techniques used for meningioma preoperative differentiation and intraoperative monitoring;
6) Surgical intervention for meningioma.
7) Modeling meningioma: patient-derived xenografts and genetically engineered mouse models.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
