{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T05:31:20Z","timestamp":1791955880686,"version":"4.3.4"},"reference-count":68,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,4]]},"abstract":"\n The epochal developments in the treatment of meningioma\u2014microsurgery, skull base techniques, and radiation therapy\u2014will be appended to include the rational application of targeted and immune therapeutics, previously ill-fitting concepts for a tumor that has traditionally been a regarded as a surgical disease. The genomic and immunological architecture of these tumors continues to be defined in ever-greater detail. Grade I meningiomas are driven by\n NF2<\/jats:italic>\n alterations or mutations in\n AKT1<\/jats:italic>\n ,\n SMO, TRAF7, PIK3CA, KLF4, POLR2A, SUFU,<\/jats:italic>\n and\n SMARCB1<\/jats:italic>\n . Higher-grade tumors, however, are driven nearly exclusively by\n NF2\/chr22<\/jats:italic>\n loss and are marked by infrequent targetable mutations, although they may harbor a greater mutation burden overall.\n TERT<\/jats:italic>\n mutations may be more common in tumors that progress in histological grade;\n SMARCE1<\/jats:italic>\n alteration has become a signature of the clear cell subtype; and\n BAP1<\/jats:italic>\n in rhabdoid variants may confer sensitivity to pharmacological inhibition. Compared with grade I meningiomas, the most prominent alteration in grade II and III meningiomas is a significant increase in chromosomal gains and losses, or copy number alterations, which may have behavioral implications. Furthermore, integrated genomic analyses suggest phenotypic subgrouping by methylation profile and a specific role for PRC2 complex activation. Lastly, there exists a complex phylogenetic relationship among recurrent high-grade tumors, which continues to underscore a role for the most traditional therapy in our arsenal: surgery.\n <\/jats:p>","DOI":"10.3171\/2017.12.focus17756","type":"journal-article","created":{"date-parts":[[2018,4,1]],"date-time":"2018-04-01T03:31:08Z","timestamp":1522553468000},"page":"E2","source":"Crossref","is-referenced-by-count":35,"title":["High-grade meningiomas: biology and implications"],"prefix":"10.3171","volume":"44","author":[{"given":"Wenya Linda","family":"Bi","sequence":"first","affiliation":[{"name":"Center for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, Massachusetts; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vikram C.","family":"Prabhu","sequence":"additional","affiliation":[{"name":"Departments of Neurological Surgery and Radiation Oncology, Loyola University Medical Center, Chicago, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian F.","family":"Dunn","sequence":"additional","affiliation":[{"name":"Center for Skull Base and Pituitary Surgery, Department of Neurosurgery, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, Massachusetts; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1","series-title":"Neuro Oncol","first-page":"649","article-title":"Oncogenic PI3K mutations are as common as AKT1 and SMO mutations in meningioma","volume":"18","author":"Abedalthagafi M","year":"2016","unstructured":"Abedalthagafi M, Bi WL, Aizer AA, Merrill PH, Brewster R, Agarwalla PK, : Oncogenic PI3K mutations are as common as AKT1 and SMO mutations in meningioma. 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