Meningioma pathophysiology: Difference between revisions
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==Genetics== | ==Genetics== | ||
Genes involved in the pathogenesis of meningioma include:<ref name="pmid27624470">{{cite journal| author=Yuzawa S, Nishihara H, Tanaka S| title=Genetic landscape of meningioma. | journal=Brain Tumor Pathol | year= 2016 | volume= 33 | issue= 4 | pages= 237-247 | pmid=27624470 | doi=10.1007/s10014-016-0271-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27624470 }} </ref><ref name="ComminsAtkinson2007">{{cite journal|last1=Commins|first1=Deborah L.|last2=Atkinson|first2=Roscoe D.|last3=Burnett|first3=Margaret E.|title=Review of meningioma histopathology|journal=Neurosurgical Focus|volume=23|issue=4|year=2007|pages=E3|issn=1092-0684|doi=10.3171/FOC-07/10/E3}}</ref><ref name="pmid23307326">{{cite journal| author=Balik V, Srovnal J, Sulla I, Kalita O, Foltanova T, Vaverka M et al.| title=MEG3: a novel long noncoding potentially tumour-suppressing RNA in meningiomas. | journal=J Neurooncol | year= 2013 | volume= 112 | issue= 1 | pages= 1-8 | pmid=23307326 | doi=10.1007/s11060-012-1038-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23307326 }} </ref><ref name="pmid16103061">{{cite journal| author=Lusis EA, Watson MA, Chicoine MR, Lyman M, Roerig P, Reifenberger G et al.| title=Integrative genomic analysis identifies NDRG2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive meningioma. | journal=Cancer Res | year= 2005 | volume= 65 | issue= 16 | pages= 7121-6 | pmid=16103061 | doi=10.1158/0008-5472.CAN-05-0043 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16103061 }} </ref><ref name="pmid20607352">{{cite journal| author=Skiriute D, Tamasauskas S, Asmoniene V, Saferis V, Skauminas K, Deltuva V et al.| title=Tumor grade-related NDRG2 gene expression in primary and recurrent intracranial meningiomas. | journal=J Neurooncol | year= 2011 | volume= 102 | issue= 1 | pages= 89-94 | pmid=20607352 | doi=10.1007/s11060-010-0291-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20607352 }} </ref> | Genes involved in the pathogenesis of meningioma include:<ref name="pmid27624470">{{cite journal| author=Yuzawa S, Nishihara H, Tanaka S| title=Genetic landscape of meningioma. | journal=Brain Tumor Pathol | year= 2016 | volume= 33 | issue= 4 | pages= 237-247 | pmid=27624470 | doi=10.1007/s10014-016-0271-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27624470 }} </ref><ref name="ComminsAtkinson2007">{{cite journal|last1=Commins|first1=Deborah L.|last2=Atkinson|first2=Roscoe D.|last3=Burnett|first3=Margaret E.|title=Review of meningioma histopathology|journal=Neurosurgical Focus|volume=23|issue=4|year=2007|pages=E3|issn=1092-0684|doi=10.3171/FOC-07/10/E3}}</ref><ref name="pmid23307326">{{cite journal| author=Balik V, Srovnal J, Sulla I, Kalita O, Foltanova T, Vaverka M et al.| title=MEG3: a novel long noncoding potentially tumour-suppressing RNA in meningiomas. | journal=J Neurooncol | year= 2013 | volume= 112 | issue= 1 | pages= 1-8 | pmid=23307326 | doi=10.1007/s11060-012-1038-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23307326 }} </ref><ref name="pmid16103061">{{cite journal| author=Lusis EA, Watson MA, Chicoine MR, Lyman M, Roerig P, Reifenberger G et al.| title=Integrative genomic analysis identifies NDRG2 as a candidate tumor suppressor gene frequently inactivated in clinically aggressive meningioma. | journal=Cancer Res | year= 2005 | volume= 65 | issue= 16 | pages= 7121-6 | pmid=16103061 | doi=10.1158/0008-5472.CAN-05-0043 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16103061 }} </ref><ref name="pmid20607352">{{cite journal| author=Skiriute D, Tamasauskas S, Asmoniene V, Saferis V, Skauminas K, Deltuva V et al.| title=Tumor grade-related NDRG2 gene expression in primary and recurrent intracranial meningiomas. | journal=J Neurooncol | year= 2011 | volume= 102 | issue= 1 | pages= 89-94 | pmid=20607352 | doi=10.1007/s11060-010-0291-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20607352 }} </ref><ref name="pmid23377182">{{cite journal| author=Smith MJ, O'Sullivan J, Bhaskar SS, Hadfield KD, Poke G, Caird J et al.| title=Loss-of-function mutations in SMARCE1 cause an inherited disorder of multiple spinal meningiomas. | journal=Nat Genet | year= 2013 | volume= 45 | issue= 3 | pages= 295-8 | pmid=23377182 | doi=10.1038/ng.2552 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23377182 }} </ref> | ||
*Neurofibromatosis 2 (NF2) gene on chromosome 22 | *Neurofibromatosis 2 (NF2) gene on chromosome 22 | ||
*MEG3 (maternally expressed gene 3): Loss of expression, genomic DNA deletion, and promoter methylation on chromosome 14q32. | *MEG3 (maternally expressed gene 3): Loss of expression, genomic DNA deletion, and promoter methylation on chromosome 14q32. | ||
*NDRG2 (N-Myc downstream-regulated gene 2): Down regulation of this gene expression at the mRNA level is associated with the malignant progression and predisposition to recurrence of meningiomas. | *NDRG2 (N-Myc downstream-regulated gene 2): Down regulation of this gene expression at the mRNA level is associated with the malignant progression and predisposition to recurrence of meningiomas. | ||
*SMARCE1 (SWI/SNF chromatin-remodeling complex subunit gene): Heterozygous loss-of-function mutation. Its is commonly seen in meningiomas with clear cell histology and those located in the spine. | |||
*TRAF7 | *TRAF7 | ||
*AKT1 | *AKT1 | ||
Revision as of 16:41, 19 April 2019
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Meningioma pathophysiology On the Web |
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Risk calculators and risk factors for Meningioma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Haytham Allaham, M.D. [2]
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.[1][2][3] The majority of meningiomas are benign. Development of meningioma is the result of multiple genetic mutations The majority of meningioma cases involve a deletion of the neurofibromatosis 2 gene located on chromosome 22. On gross pathology, a gray, well-circumscribed, dome-shaped mass is a characteristic finding of meningioma. On microscopic histopathological analysis, whorled appearance, calcification, and psammoma bodies are characteristic findings of meningioma.[4]
Pathogenesis
- Meningiomas are the most common benign tumors of the brain. They are also the most common nonglial brain tumors.[5]
- 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.[6]
- Meningiomas are commonly found in the base of the skull and perivenous sinuses due to the abundance of arachnoid cap cells in these sites. They are usually non-infilterative.[5]
- The majority of meningiomas are benign (90%), about 6% are atypical, and 2% are malignant.[5]
- Some meningiomas may be positive for progesterone receptors on histological examination. This can lead to increased tumor size and symptom burden during pregnancy and the luteal phase of the menstural cycle.[5]
- Meningiomas may possess receptors for platelet derived growth factor, vascular endothelial growth factor (VEGF), glucocorticoid, and epidermal growth factor.[5]
- Meningiomas can be found anywhere in the central nervous system, with its most frequent distribution as follows: parasagittal (20.8%), then convexity (15.2%), and tuberculum sellae (12.8%).[7]
- The symptoms of meningioma can be flared by water retention, engorgement of blood vessels, and the presence of sex hormone receptors on tumor cells.[5]
- A meningioma can be localized in the following areas: sphenoid ridge, olfactory groove, falx, lateral ventriculi, tentorium, the middle fossa, the orbit, the spinal channel, the Sylvian fissure, extracalvarial, multiple localization, the pontocerebral angle, the sphenoidal plane, and the foramen magnum.[7]
- The characteristics of a meningioma can be determined based on histopathological variables like tumor gradient, histological subtype, proliferative index, and invasiveness of a tumor to the brain.[7]
- The characterization of a meningioma being malignant is based on one or more of the following criteria: brain invasion, frank anaplasia, and distant metastasis[8]
Genetics
Genes involved in the pathogenesis of meningioma include:[9][8][10][11][12][13]
- Neurofibromatosis 2 (NF2) gene on chromosome 22
- MEG3 (maternally expressed gene 3): Loss of expression, genomic DNA deletion, and promoter methylation on chromosome 14q32.
- NDRG2 (N-Myc downstream-regulated gene 2): Down regulation of this gene expression at the mRNA level is associated with the malignant progression and predisposition to recurrence of meningiomas.
- SMARCE1 (SWI/SNF chromatin-remodeling complex subunit gene): Heterozygous loss-of-function mutation. Its is commonly seen in meningiomas with clear cell histology and those located in the spine.
- TRAF7
- AKT1
- KLF4
- SMO
- PIK3CA
Associated Conditions
Conditions associated with meningioma include:[14]
- Neurofibromatosis type 2
- Nevoid basal cell carcinoma syndrome
- Multiple endocrine neoplasia 1 (MEN1)
- Cowden syndrome
- Werner syndrome
- BAP1 tumor predisposition syndrome
- Rubinstein-Taybi syndrome
- Familial meningiomatosis
Gross Pathology
- On gross pathology, a gray, well-circumscribed, dome-shaped mass is a characteristic finding of meningioma.[1]
Microscopic Pathology
- 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
- 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:[8]
- Positive for vimentin
- Negative for cytokeratin
- Weak or negative staining for S 100 protein
- Focal membranous positivity for EMA
References
- ↑ 1.0 1.1 Meningioma. Wikipedia(2015) https://en.wikipedia.org/wiki/Meningioma#cite_note-pmid7731706-9 Accessed on September, 25 2015
- ↑ Meningioma. Canadian Cancer Society http://www.cancer.ca/en/cancer-information/cancer-type/brain-spinal/brain-and-spinal-tumours/meningioma/?region=mb September, 25 2015
- ↑ Meningeoma. Radiopaedia(2015)http://radiopaedia.org/articles/meningioma Accessed on September, 25 2015
- ↑ Meningioma. Libre Pathology(2015) http://librepathology.org/wiki/index.php/Meningioma#Quick_overview accessed on September, 25 2015
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 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.
- ↑ 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
- ↑ 7.0 7.1 7.2 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.
- ↑ 8.0 8.1 8.2 8.3 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Image courtesy of Dr Dharam Ramnani Radiopaedia(original file "here"). Creative Commons BY-SA-NC
- ↑ 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.