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By Marzenna Wiranowska, Visit Amazon's Frank D. Vrionis Page, search results, Learn about Author Central, Frank D. Vrionis,

ISBN-10: 162618089X

ISBN-13: 9781626180895

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The phosphatidylinositol 3-kinases (PI3K) are a family of enzymes that relay important cellular growth control signals. In half of GBMs there is either a PI3K-activating mutation or a deletion/mutation of its negative regulator PTEN. A mutated insulin-mediated activator of PI3K kinase, insulin substrate receptor-1 has also been reported [12]. This observation is confirmed in a study by Gallia et al. [12]. The authors found that this mutation occurs in a significant number of human glioblastomas, further indicating that therapeutic targeting of this pathway in glioblastomas is of value.

Journal of neurosurgery. 1991;74(3):399-406. Epub 1991/03/01. Bigner DD, McLendon RE, Bruner JM. Russell and Rubinstein's pathology of tumors of the nervous system. 7th ed. London. New York, NY: Hodder Arnold; Distributed in the United States of America by Oxford University Press; 2006. xxiii, 1132 p. p. Bailey P, Cushing H. A classification of the tumors of the glioma group on a histogenetic basis with a correlated study of prognosis. B. Lippincott Company; 1926. 3 p. , 175 p. incl. , tables, diagrs.

Recent studies highlight the importance of BRAF alterations resulting in mitogen activated protein kinase (MAK/ERK) pathway activation in low-grade CNS tumors [28]. For this purpose, Lin et al. studied 106 low-grade CNS neoplasms in a cohort of primarily pediatric patients to identify the prevalence and clinicopathologic significance of these alterations [28]. They found that BRAF alterations included KIAA1549:BRAF fusions in 51 (48%) and BRAF exon 15 (BRAFV600E) point mutations in 8 (8%). These alterations were more common in tumors arising from the cerebellum and optic pathways.

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