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

by: Victoria E. Clark, E. Zeynep Erson-Omay, Akdes Serin, Jun Yin, Justin Cotney, Koray Özduman, Timuçin Avşar, Jie Li, Phillip B. Murray, Octavian Henegariu, Saliha Yilmaz, Jennifer M. Günel, Geneive Carrión-Grant, Baran Yılmaz, Conor Grady, Bahattin Tanrıkulu, Mehmet Bakırcıoğlu, Hande Kaymakçalan, Ahmet O. Caglayan, Leman Sencar, Emre Ceyhun, A. Fatih Atik, Yaşar Bayri, Hanwen Bai, Luis E. Kolb, Ryan M. Hebert, S. Bulent Omay, Ketu Mishra-Gorur, Murim Choi, John D. Overton, Eric C. Holland, Shrikant Mane, Matthew W. State, Kaya Bilgüvar, Joachim M. Baehring, Philip H. Gutin, Joseph M. Piepmeier, Alexander Vortmeyer, Cameron W. Brennan, M. Necmettin Pamir, Türker Kılıç, Richard P. Lifton, James P. Noonan, Katsuhito Yasuno, Murat Günel
Science, Vol. 339, No. 6123. (01 March 2013), pp. 1077-1080, doi:10.1126/science.1233009  Key: citeulike:12093277

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Abstract

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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