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DOI: 10.1055/s-2007-984451
© Georg Thieme Verlag KG Stuttgart · New York
Further Evidence for a Somatic KRAS Mutation in a Pilocytic Astrocytoma
Publication History
received 15.3.2007
accepted 15.5.2007
Publication Date:
22 August 2007 (online)
Abstract
Astrocytomas are the most common brain tumors of childhood. However, knowledge of the molecular etiology of astrocytomas WHO grade I and II is limited. Germline mutations in the Ras-guanosine triphosphatase-activating protein, neurofibromin, in individuals with neurofibromatosis type I predispose to pilocytic astrocytomas. This association suggests that constitutive activation of the Ras signaling pathway plays a fundamental role in astrocytoma development. We screened 25 WHO I and II astrocytomas for mutations of PTPN11, NRAS, KRAS, and HRAS genes and identified the somatic G12A KRAS mutation in one pilocytic astrocytoma. These data suggest that Ras is rarely mutated in these tumors. Analyzed astrocytomas without mutations in Ras or neurofibromin may harbor mutations in other proteins of this pathway leading to hyperactive Ras signaling.
Key words
Astrocytoma - RAS - tumor
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Correspondence
Prof. Dr. H. Omran
Department of Pediatric Neurology and Muscle Disorders
University Hospital Freiburg
Mathildenstr. 1
79106 Freiburg
Germany
Phone: +49/761/270 43 65
Fax: +49/761/270 43 65
Email: heymut.omran@uniklinik-freiburg.de