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
AUTHORS (45)
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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