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      An overview of meningiomas

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          Abstract

          <p class="first" id="d4659962e236">Meningiomas are the most common primary intracranial tumor. Important advances are occurring in meningioma research. These are expected to accelerate, potentially leading to impactful changes on the management of meningiomas in the near and medium term. This review will cover the histo- and molecular pathology of meningiomas, including recent 2016 updates to the WHO classification of CNS tumors. We will discuss clinical and radiographic presentation and therapeutic management. Surgery and radiotherapy, the two longstanding primary therapeutic modalities, will be discussed at length. In addition, data from prior and ongoing investigations of other treatment modalities, including systemic and targeted therapies, will be covered. This review will quickly update the reader on the contemporary management and future directions in meningiomas. </p><p id="d4659962e238"> <img alt="" class="inline-figure" src="/document_file/2bf6dfef-0f5f-4c11-b37c-14f53042b1d8/PubMedCentral/image/fon-14-2161-GA.jpg"/> </p>

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          The recurrence of intracranial meningiomas after surgical treatment.

          D. Simpson (1957)
          Article 0 comments Cited 371 times – based on 0 reviews     Review now
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            Genomic analysis of non-NF2 meningiomas reveals mutations in TRAF7, KLF4, AKT1, and SMO.

            Victoria E. Clark, E Zeynep Erson-Omay, Akdes Serin … (2013)
            We report genomic analysis of 300 meningiomas, the most common primary brain tumors, leading to the discovery of mutations in TRAF7, a proapoptotic E3 ubiquitin ligase, in nearly one-fourth of all meningiomas. Mutations in TRAF7 commonly occurred with a recurrent mutation (K409Q) in KLF4, a transcription factor known for its role in inducing pluripotency, or with AKT1(E17K), a mutation known to activate the PI3K pathway. SMO mutations, which activate Hedgehog signaling, were identified in ~5% of non-NF2 mutant meningiomas. These non-NF2 meningiomas were clinically distinctive-nearly always benign, with chromosomal stability, and originating from the medial skull base. In contrast, meningiomas with mutant NF2 and/or chromosome 22 loss were more likely to be atypical, showing genomic instability, and localizing to the cerebral and cerebellar hemispheres. Collectively, these findings identify distinct meningioma subtypes, suggesting avenues for targeted therapeutics.
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              Epidemiology and etiology of meningioma

              Joseph Wiemels, Margaret R. Wrensch, Elizabeth Claus (2010)
              Although most meningiomas are encapsulated and benign tumors with limited numbers of genetic aberrations, their intracranial location often leads to serious and potentially lethal consequences. They are the most frequently diagnosed primary brain tumor accounting for 33.8% of all primary brain and central nervous system tumors reported in the United States between 2002 and 2006. Inherited susceptibility to meningioma is suggested both by family history and candidate gene studies in DNA repair genes. People with certain mutations in the neurofibromatosis gene (NF2) have a very substantial increased risk for meningioma. High dose ionizing radiation exposure is an established risk factor for meningioma, and lower doses may also increase risk, but which types and doses are controversial or understudied. Because women are twice as likely as men to develop meningiomas and these tumors harbor hormone receptors, an etiologic role for hormones (both endogenous and exogenous) has been hypothesized. The extent to which immunologic factors influence meningioma etiology has been largely unexplored. Growing emphasis on brain tumor research coupled with the advent of new genetic and molecular epidemiologic tools in genetic and molecular epidemiology promise hope for advancing knowledge about the causes of intra-cranial meningioma. In this review, we highlight current knowledge about meningioma epidemiology and etiology and suggest future research directions.
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                Author and article information

                Journal
                Title: Future Oncology
                Abbreviated Title: Future Oncology
                Publisher: Future Medicine Ltd
                ISSN (Print): 1479-6694
                ISSN (Electronic): 1744-8301
                Publication date Created: September 2018
                Publication date (Print): September 2018
                Volume: 14
                Issue: 21
                Pages: 2161-2177
                Affiliations
                [1 ]Department of Neurological Surgery, University of California San Francisco, 400 Parnassus Ave., San Francisco, CA 94143, USA
                [2 ]Department of Pathology, Northwestern University, IL 60611, USA
                [3 ]Lou &amp; Jean Malnati Brain Tumor Institute at the Lurie Comprehensive Cancer Center, Northwestern University, IL 60611, USA
                [4 ]Department of Radiation Oncology, Northwestern University, IL 60611, USA
                [5 ]Section of Neurosurgery, University of Chicago, 5841 S. Maryland Ave., Chicago, IL 60637, USA
                [6 ]Department of Neurosurgery, Northwestern University, IL 60611, USA
                [7 ]Department of Neurology, Northwestern University, 710 North Lake Shore Drive, Abbott Hall 1114, Chicago, IL 60611, USA
                Article
                DOI: 10.2217/fon-2018-0006
                PMC ID: 6123887
                PubMed ID: 30084265
                SO-VID: 4ff105fe-788b-462f-9dbc-2aa705bea6be
                Copyright © © 2018
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