Meningioma pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Odukwe, M.D. [2] Haytham Allaham, M.D. [3]

Overview

Meningioma arises from the arachnoid "cap" cells, which are normally involved in the protection of the central nervous system by forming a thick envelope of meninges around the brain and spinal cord. The majority of meningiomas are benign. They can be found anywhere in the central nervous system but are most commonly seen in the parasagittal, convexity and turbeculum sellae areas. There may be genetic mutations involved in the development of a meningioma, some of the genes involved includes NF2, MEG3, NDRG2, and SMARCE1. Multiple endocrine neoplasia 1, cowden syndrome, werner syndrome and neurofibromatosis 2 are some of the conditions that may be associated with meningioma. On microscopic pathology, some of the characteristic findings of a meningioma include mitotic figures, necrosis, interdigitating processes, and brain invasion. Most meningiomas are positive for vimentin and negative for cytokeratin.

Pathogenesis

Genetics

Genes involved in the pathogenesis of meningioma include:[5][4][6][7][8][9][10][11]

Associated Conditions

Conditions associated with meningioma include:[12]

Gross Pathology

  • On gross pathology, a gray, well-circumscribed, dome-shaped mass is a characteristic finding of meningioma.[13]


Microscopic Pathology

  • On microscopic pathology, characteristic findings of meningioma include:[4][14]
  • Interdigitating processes and intercellular junctions
  • Small foci of necrosis surrounded by pseudopalisading tumor cells in nonembolized atypical meningiomas
  • Necrosis occurring in large geographic areas with a quick line demarcating it from viable tissues in embolized menigiomas
  • Prominent macronucleoli in the perinecrotic areas in embolized meningiomas
  • Mitotic figures (low in benign cases and high in malignant and atypical cases)
  • Brain invasion histologically seen as a finger-like, a tongue-like, or a knobby protrusion into the tissue
  • Small cells with a high nuclear:cytoplasmic ratio
  • Prominent nucleoli
  • Uninterrupted patternless or sheet-like growth
  • Increased cellularity
  • The following immunohistochemistry profile can be used to support the diagnosis of meningioma:[4]
  • Positive for vimentin
  • Negative for cytokeratin
  • Weak or negative staining for S 100 protein
  • Focal membranous positivity for EMA
Histology slide showing meningioma with prominent mitosis source:Jensflorian-wikimedia commons


Histology slide showing secretory meningioma source:Jensflorian-wikimedia commons



References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Gurcay AG, Bozkurt I, Senturk S, Kazanci A, Gurcan O, Turkoglu OF; et al. (2018). "Diagnosis, Treatment, and Management Strategy of Meningioma during Pregnancy". Asian J Neurosurg. 13 (1): 86–89. doi:10.4103/1793-5482.181115. PMC 5820904. PMID 29492130.
  2. Wiemels J, Wrensch M, Claus EB (2010) Epidemiology and etiology of meningioma. J Neurooncol 99 (3):307-14. DOI:10.1007/s11060-010-0386-3 PMID: 20821343
  3. 3.0 3.1 3.2 Sumkovski R, Micunovic M, Kocevski I, Ilievski B, Petrov I (2019). "Surgical Treatment of Meningiomas - Outcome Associated With Type of Resection, Recurrence, Karnofsky Performance Score, Mitotic Count". Open Access Maced J Med Sci. 7 (1): 56–64. doi:10.3889/oamjms.2018.503. PMC 6352459. PMID 30740161.
  4. 4.0 4.1 4.2 4.3 Commins, Deborah L.; Atkinson, Roscoe D.; Burnett, Margaret E. (2007). "Review of meningioma histopathology". Neurosurgical Focus. 23 (4): E3. doi:10.3171/FOC-07/10/E3. ISSN 1092-0684.
  5. Yuzawa S, Nishihara H, Tanaka S (2016). "Genetic landscape of meningioma". Brain Tumor Pathol. 33 (4): 237–247. doi:10.1007/s10014-016-0271-7. PMID 27624470.
  6. Balik V, Srovnal J, Sulla I, Kalita O, Foltanova T, Vaverka M; et al. (2013). "MEG3: a novel long noncoding potentially tumour-suppressing RNA in meningiomas". J Neurooncol. 112 (1): 1–8. doi:10.1007/s11060-012-1038-6. PMID 23307326.
  7. Lusis EA, Watson MA, Chicoine MR, Lyman M, Roerig P, Reifenberger G; et al. (2005). "Integrative genomic analysis identifies NDRG2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive meningioma". Cancer Res. 65 (16): 7121–6. doi:10.1158/0008-5472.CAN-05-0043. PMID 16103061.
  8. Skiriute D, Tamasauskas S, Asmoniene V, Saferis V, Skauminas K, Deltuva V; et al. (2011). "Tumor grade-related NDRG2 gene expression in primary and recurrent intracranial meningiomas". J Neurooncol. 102 (1): 89–94. doi:10.1007/s11060-010-0291-9. PMID 20607352.
  9. Smith MJ, O'Sullivan J, Bhaskar SS, Hadfield KD, Poke G, Caird J; et al. (2013). "Loss-of-function mutations in SMARCE1 cause an inherited disorder of multiple spinal meningiomas". Nat Genet. 45 (3): 295–8. doi:10.1038/ng.2552. PMID 23377182.
  10. van den Munckhof P, Christiaans I, Kenter SB, Baas F, Hulsebos TJ (2012). "Germline SMARCB1 mutation predisposes to multiple meningiomas and schwannomas with preferential location of cranial meningiomas at the falx cerebri". Neurogenetics. 13 (1): 1–7. doi:10.1007/s10048-011-0300-y. PMID 22038540.
  11. Goutagny S, Nault JC, Mallet M, Henin D, Rossi JZ, Kalamarides M (2014). "High incidence of activating TERT promoter mutations in meningiomas undergoing malignant progression". Brain Pathol. 24 (2): 184–9. doi:10.1111/bpa.12110. PMID 24261697.
  12. Kerr K, Qualmann K, Esquenazi Y, Hagan J, Kim DH (2018). "Familial Syndromes Involving Meningiomas Provide Mechanistic Insight Into Sporadic Disease". Neurosurgery. 83 (6): 1107–1118. doi:10.1093/neuros/nyy121. PMC 6235681. PMID 29660026.
  13. Meningioma. Wikipedia(2015) https://en.wikipedia.org/wiki/Meningioma#cite_note-pmid7731706-9 Accessed on September, 25 2015
  14. Shibuya M (2015). "Pathology and molecular genetics of meningioma: recent advances". Neurol Med Chir (Tokyo). 55 (1): 14–27. doi:10.2176/nmc.ra.2014-0233. PMC 4533397. PMID 25744347.

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