Genomic Analysis of Non- NF2 Meningiomas Reveals Mutations in TRAF7 , KLF4 , AKT1 , and SMO

Adult Male Neurofibromatosis 2 General Science & Technology Chromosomes, Human, Pair 22 DNA Mutational Analysis Kruppel-Like Transcription Factors Chromosomes Genomic Instability G-Protein-Coupled Kruppel-Like Factor 4 Rare Diseases Genes, Neurofibromatosis 2 Receptors Genetics 80 and over Meningeal Neoplasms Humans Cancer Aged Aged, 80 and over Biomedical and Clinical Sciences Brain Neoplasms Human Genome Neurosciences Genomics Biological Sciences Middle Aged Smoothened Receptor Tumor Necrosis Factor Receptor-Associated Peptides and Proteins Brain Disorders 3. Good health Brain Cancer Genes Mutation Female Pair 22 Neoplasm Grading Meningioma Proto-Oncogene Proteins c-akt Human
DOI: 10.1126/science.1233009 Publication Date: 2013-01-25T02:38:41Z
ABSTRACT
Genetic Clues to Meningioma Meningiomas are the most common primary brain tumors in adults. Located within the layer of tissue covering the brain, these tumors are usually slow-growing and benign but can cause serious neurological complications. About half of these tumors have mutations in the neurofibromin 2 gene ( NF2 ). To identify other genes that contribute to meningioma pathogenesis, Clark et al. (p. 1077 , published online 24 January) performed genome sequence analysis on 300 tumors. Meningiomas fell into two general classes: benign tumors located at the skull base—which tend to harbor mutations in the TRAF7, KLF4, AKT1 , and SMO genes—and higher-grade tumors located in the cerebral and cerebellar hemispheres harbor mutations in NF2.
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