Meningioma genomics: A therapeutic challenge for clinicians

dc.contributor.authorMoussalem, Charbel K.
dc.contributor.authorMassaad, Elie
dc.contributor.authorMinassian, Georges B.
dc.contributor.authorFtouni, Louna
dc.contributor.authorBsat, Shadi Abdelatif
dc.contributor.authorEl Houshiemy, Mohamad Nabih
dc.contributor.authorAlomari, Safwan Omar
dc.contributor.authorSarieddine, Rana
dc.contributor.authorKobeissy, Firas H.
dc.contributor.authorOmeis, Ibrahim A.
dc.contributor.departmentSurgery
dc.contributor.departmentBiochemistry and Molecular Genetics
dc.contributor.departmentDivision of Neurosurgery
dc.contributor.facultyFaculty of Medicine (FM)
dc.contributor.institutionAmerican University of Beirut
dc.date.accessioned2025-01-24T12:13:45Z
dc.date.available2025-01-24T12:13:45Z
dc.date.issued2021
dc.description.abstractMeningiomas are amongst the most commonly encountered intracranial tumors. The majority of these tumors arise intracranially, and the remaining incidents occur along the spinal cord. Meningiomas tend to grow gradually, with many tumors arising in inaccessible locations. Such sporadic behavior poses a therapeutic challenge to clinicians, causing incomplete tumor resections that often lead to recurrence. Therefore, ongoing research seeks to find alternative systematic treatments for meningiomas, with gene-based therapeutics of high interest. Subsequently, genetic studies characterized frequent somatic mutations in NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA. These genes are communally exhibited in 80% of sporadic meningiomas. In addition, other genes such as the DUSP family, the NR4 family, CMKOR, and FOSL2, have been identified as key players in spinal meningiomas. In this perspective, we aim to investigate current genetic-based studies, with the ongoing research mainly focused on the above NF2, TRAF7, KLF4, AKT1, SMO, and PIK3CA genes and their involved pathways. In addition, this perspective can serve as a potential cornerstone for future genetic analyses of meningioma cases. © 2021 The Author(s). Published by IMR Press.
dc.identifier.doihttps://doi.org/10.31083/j.jin2002049
dc.identifier.eid2-s2.0-85111141098
dc.identifier.pmid34258948
dc.identifier.urihttp://hdl.handle.net/10938/33093
dc.language.isoen
dc.publisherIMR Press Limited
dc.relation.ispartofJournal of Integrative Neuroscience
dc.sourceScopus
dc.subjectCranial meningioma
dc.subjectGene-targeting therapy
dc.subjectGenetics
dc.subjectNeurology
dc.subjectSomatic mutations
dc.subjectSpinal meningioma
dc.subjectHumans
dc.subjectMeningeal neoplasms
dc.subjectMeningioma
dc.subjectAntineoplastic agent
dc.subjectKruppel like factor 4
dc.subjectMerlin
dc.subjectPhosphatidylinositol 3 kinase
dc.subjectProtein
dc.subjectSmoothened protein
dc.subjectTumor necrosis factor receptor associated factor 7
dc.subjectUnclassified drug
dc.subjectCancer prognosis
dc.subjectCell proliferation
dc.subjectChromosome 22
dc.subjectChromosome aberration
dc.subjectDna methylation
dc.subjectEnzyme activation
dc.subjectEpigenetics
dc.subjectGene deletion
dc.subjectGene mutation
dc.subjectGenetic analysis
dc.subjectGenomics
dc.subjectHeterozygosity loss
dc.subjectHomozygosity
dc.subjectHuman
dc.subjectIntracranial tumor
dc.subjectNonhuman
dc.subjectPromoter region
dc.subjectProtein analysis
dc.subjectProtein expression
dc.subjectReview
dc.subjectSignal transduction
dc.subjectTumor growth
dc.titleMeningioma genomics: A therapeutic challenge for clinicians
dc.typeReview

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