title: Genetic/molecular alterations of meningiomas and the signaling pathways targeted.
abstract: Meningiomas are usually considered to be benign central nervous system tumors; however, they show heterogenous clinical, histolopathological and cytogenetic features associated with a variable outcome. In recent years important advances have been achieved in the identification of the genetic/molecular alterations of meningiomas and the signaling pathways involved. Thus, monosomy 22, which is often associated with mutations of the NF2 gene, has emerged as the most frequent alteration of meningiomas; in addition, several other genes (e.g., AKT1, KLF4, TRAF7, SMO) and chromosomes have been found to be recurrently altered often in association with more complex karyotypes and involvement of multiple signaling pathways. Here we review the current knowledge about the most relevant genes involved and the signaling pathways targeted by such alterations. In addition, we summarize those proposals that have been made so far for classification and prognostic stratification of meningiomas based on their genetic/genomic features.
authors.affiliation: Centre for Neurosciences and Cell Biology and Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.|Centre for Cancer Research (CIC-IBMCC, CSIC/USAL, IBSAL) and Department of Medicine, University of Salamanca, Salamanca, Spain.
authors.forename: Patrícia
authors.initials: P
authors.lastname: Domingues
authors.affiliation: Centre for Cancer Research (CIC-IBMCC, CSIC/USAL, IBSAL) and Department of Medicine, University of Salamanca, Salamanca, Spain.
authors.forename: María
authors.initials: M
authors.lastname: González-Tablas
authors.affiliation: Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: Álvaro
authors.initials: Á
authors.lastname: Otero
authors.affiliation: Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: Daniel
authors.initials: D
authors.lastname: Pascual
authors.affiliation: Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: Laura
authors.initials: L
authors.lastname: Ruiz
authors.affiliation: Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: David
authors.initials: D
authors.lastname: Miranda
authors.affiliation: Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: Pablo
authors.initials: P
authors.lastname: Sousa
authors.affiliation: Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: Jesús María
authors.initials: JM
authors.lastname: Gonçalves
authors.affiliation: Centre for Neurosciences and Cell Biology and Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.
authors.forename: María Celeste
authors.initials: MC
authors.lastname: Lopes
authors.affiliation: Centre for Cancer Research (CIC-IBMCC, CSIC/USAL, IBSAL) and Department of Medicine, University of Salamanca, Salamanca, Spain.
authors.forename: Alberto
authors.initials: A
authors.lastname: Orfao
authors.affiliation: Centre for Cancer Research (CIC-IBMCC, CSIC/USAL, IBSAL) and Department of Medicine, University of Salamanca, Salamanca, Spain.|Neurosurgery Service, University Hospital of Salamanca, Salamanca, Spain.
authors.forename: María Dolores
authors.initials: MD
authors.lastname: Tabernero
mesh_terms: D002892:Chromosomes, Human, Pair 22 / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D000090062:Kruppel-Like Factor 4; D008577:Meningeal Neoplasms / Q000235:genetics* / Q000473:pathology; D008579:Meningioma / Q000235:genetics* / Q000473:pathology; D008957:Models, Genetic; D009006:Monosomy; D025581:Neurofibromin 2 / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics*
chemical_list: C000715467:KLF4 protein, human; D000090062:Kruppel-Like Factor 4; D025581:Neurofibromin 2
keywords: chromosome 22; genetic/molecular alteration; meningioma; signal pathways