skull_base_meningioma

Skull base meningioma

Skull base meningioma epidemiology

see Anterior skull base meningioma.

see Central skull base meningioma.

see Middle skull base meningioma.

see Posterior fossa meningioma.


see Pediatric Skull Base Meningioma.

Genetic aberrations (TRAF7, KLF4, AKT1, and SMO) and the effects of genetic aberrations on the expression of immune checkpoint inhibitory molecules (PD-L1, IDO, and TDO2) in skull base meningiomas are still unclear.

Genetic alterations in the four genes were identified in 92 skull base meningiomas by Sanger sequencing. The expression differences in immune checkpoints between mutant and wild-type (WT) tumors were determined by immunohistochemistry (IHC) and Western blot (WB).

The four mutations were not concurrently detected in the patients with skull base meningiomas. Among the tumors from the KLF4-mutated group, almost half were petroclival meningiomas. KLF4- and TRAF7-mutated tumors were predominantly secretory meningiomas. SMO-mutated tumors exhibited higher calcification, and half of these tumors were observed in the brain midline. Receiver operating characteristic curve analysis indicated that tumor volume can predict KLF4 and TRAF7 mutation status with high sensitivity and specificity, respectively. The IHC and WB analyses indicated that PD-L1, IDO, and TDO2 levels in tumors with TRAF7 mutations were significantly higher than those in WT tumors. Meanwhile, there was a significant difference in TDO2 between tumors with AKT1 mutations and WT tumors. Specifically, TRAF7 mutations could play a key role in skull base meningiomas by regulating the expression of inhibitory immune checkpoints and thus suppressing immune responses.

Checkpoint inhibitors may be potential strategies for targeted immunotherapies of these mutant meningiomas 1).

Efforts to achieve a radical resection with dural margin are not suitable in many cases of skull base meningiomas, because of the neurovascular structures around the tumors.

Gamma knife radiosurgery (GKRS) is well established in the management of inaccessible, recurrent, or residual benign skull base meningiomas. Most series report clinical outcome parameters and complications in the short intermediate period after radiosurgery.

GKRS offers a highly durable rate of tumor control for World Health Organization grade 1 meningioma, with an acceptably low incidence of neurological deficits. The Karnofsky Performance Scale at the time of radiosurgery serves as a reliable long-term predictor of overall outcome 2).

Peritumoral edema (PTE) in skull base meningiomas correlates to the absence of an arachnoid plane and difference in outcome.

A subset of benign (WHO grade I) skull base meningiomas show early progression/recurrence (P/R) in the first years after surgical resection.

Ko et al. retrospectively investigated the preoperative CT and MR imaging features for the prediction of P/R in skull base meningiomas, with emphasis on quantitative ADC values. Only patients had postoperative MRI follow-ups for more than 1 year (at least every 6 months) were included. From October 2006 to December 2015, total 73 patients diagnosed with benign (WHO grade I) skull base meningiomas were included (median follow-up time 41 months), and 17 (23.3%) patients had P/R (median time to P/R 28 months). Skull base meningiomas with spheno-orbital location, adjacent bone invasion, high DWI, and lower ADC value/ratio were significantly associated with P/R (P < 0.05). The cut-off points of ADC value and ADC ratio for prediction of P/R are 0.83 × 10- 3 mm2/s and 1.09 respectively, with excellent area under curve (AUC) values (0.86 and 0.91) (P < 0.05). In multivariate logistic regression, low ADC values (< 0.83 × 10- 3 mm2/s) and adjacent bone invasion are high-risk factors of P/R (P < 0.05), with odds ratios of 31.53 and 17.59 respectively. The preoperative CT and MRI features for prediction of P/R offered clinically vital information for the planning of treatment in skull base meningiomas 3).

see Skull base meningioma case series.


1)
Hao S, Huang G, Feng J, Li D, Wang K, Wang L, Wu Z, Wan H, Zhang L, Zhang J. Non-NF2 mutations have a key effect on inhibitory immune checkpoints and tumor pathogenesis in skull base meningiomas. J Neurooncol. 2019 Jun 8. doi: 10.1007/s11060-019-03198-9. [Epub ahead of print] PubMed PMID: 31177425.
2)
Cohen-Inbar O, Lee CC, Schlesinger D, Xu Z, Sheehan JP. Long-Term Results of Stereotactic Radiosurgery for Skull Base Meningiomas. Neurosurgery. 2016 Jul;79(1):58-68. doi: 10.1227/NEU.0000000000001045. PubMed PMID: 26421592.
3)
Ko CC, Lim SW, Chen TY, Chen JH, Li CF, Shiue YL. Prediction of progression in skull base meningiomas: additional benefits of apparent diffusion coefficient value. J Neurooncol. 2018 Jan 20. doi: 10.1007/s11060-018-2769-9. [Epub ahead of print] PubMed PMID: 29353434.
  • skull_base_meningioma.txt
  • Last modified: 2019/06/10 13:40
  • by administrador