Meningioma recurrence

• Anlotinib therapy for recurrent and progressive atypical meningioma: A case report
• Different clinical and cytogenetic features of primary skull base meningiomas and non-skull base meningiomas
• Comparative analysis of outcomes following craniotomy and expanded endoscopic endonasal approach resection of tuberculum sellae meningiomas: a single-institution study
• Intracranial Hypotension Syndrome after Lumbar Drainage in Skull Base Surgery: Diagnosis and Correct Management
• Safety and efficacy of Cesium-131 brachytherapy for brain tumors
• Identification of incidental brain tumors in prostate cancer patients via PSMA PET/CT
• Clinical and genomic differences in supratentorial versus infratentorial NF2 mutant meningiomas
• A systematic review and individual participant data meta-analysis of gonadal steroid hormone receptors in meningioma

If a tumor returns after being resected previously, it is recommended to be resected, followed by radiotherapy in some cases. Meningiomas (benign, atypical, and malignant) recurring after standard treatment fails could be treated with hormone therapy, chemotherapy, target therapy, and calcium channel blockers ¹⁾

In Intracranial meningioma surgery, resection is considered to be the most important therapeutic step to avoid meningioma recurrence. However, resection of skull base lesions with orbital or optic nerve involvement poses a challenge due to their anatomical structure and their proximity to eloquent areas.

In a study, by Huang et al. scRNA-Seq is used to identify a unique initiating cell subpopulation (SULT1E1+ ) in high-grade meningiomas. This subpopulation modulates the polarization of M2 macrophages and promotes meningioma progression and meningioma recurrence. A novel patient-derived meningioma organoid (MO) model is established to characterize this unique subpopulation. The resulting MOs fully retain the aggressiveness of SULT1E1+ and exhibit invasiveness in the brain after orthotopic transplantation. By targeting SULT1E1+ in MOs, the synthetic compound SRT1720 is identified as a potential agent for systemic treatment and radiation sensitization. These findings shed light on the mechanism underlying the malignancy of high-grade meningiomas and provide a novel therapeutic target for refractory high-grade meningioma ²⁾.

Genomic profiling can provide an unbiased adjunct to traditional meningioma classification and provides a basis for exploring the different genetic underpinnings of tumor initiation and progression. Most importantly, the striking difference observed between sporadic and familial multiple meningiomas indicates that genomic profiling can provide valuable information for differential diagnosis of subjects with multiple meningiomas and for considering the risk for tumor occurrence in their family members ³⁾.

There are four critical histopathological variables that affect the rate of meningioma recurrence:

1. Meningioma grade

2. Meningioma histological subtype

3. Meningioma proliferation index

4. Brain invasion (see Brain invasion in atypical meningioma).

The presence of brain invasion increases the likelihood of recurrence to levels similar to atypical meningiomas (not anaplastic), ⁴⁾ but is not an indicator of malignant grade. Brain invasion in atypical meningiomas does not dictate malignant behavior. Adding the phrase “with brain invasion” is suggested to denote a higher risk of recurrence ⁵⁾

Tumor recurrence remains the major clinical complication of meningiomas, the majority of recurrences occurring among WHO grade I/benign tumors.

The MIB-1 index was evaluated as a possible predictor of meningiomas with a higher risk of recurrence ⁶⁾.

Domingues et al, found an adverse impact on patient relapse-free survival (RFS) for males, presence of brain edema, younger patients (<55 years), tumor size >50 mm, tumor localization at intraventricular and anterior cranial base areas, WHO grade II/III meningiomas, and complex karyotypes; the latter 5 variables showed an independent predictive value in multivariate analysis. Based on these parameters, a prognostic score was established for each individual case, and patients were stratified into 4 risk categories with significantly different (P < .001) outcomes. These included a good prognosis group, consisting of approximately 20% of cases, that showed a RFS of 100% ± 0% at 10 years and a very poor-prognosis group with a RFS rate of 0% ± 0% at 10 years. The prognostic impact of the scoring system proposed here was also retained when WHO grade I cases were considered separately (P < .001) ⁷⁾.