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Mutation analysis of the Ras pathway genes NRAS, HRAS, KRAS and BRAF in glioblastomas.

Authors: Knobbe, Christiane B  Reifenberger, Julia  Reifenberger, Guido 
Citation: Knobbe CB, etal., Acta Neuropathol. 2004 Dec;108(6):467-70. doi: 10.1007/s00401-004-0929-9. Epub 2004 Oct 28.
Pubmed: (View Article at PubMed) PMID:15517309
DOI: Full-text: DOI:10.1007/s00401-004-0929-9

Aberrant activation of Ras signaling is a common finding in human glioblastomas. To determine the contribution of Ras gene mutations to this aberration, we screened 94 glioblastomas for mutations in the three Ras family genes NRAS, KRAS and HRAS. All tumors were additionally analyzed for mutations in BRAF, which encodes a Ras-regulated serine/threonine kinase with oncogenic properties. Mutation analysis of the entire coding regions of NRAS and KRAS, as well as the known mutation hot-spot sites in HRAS, identified somatic point mutations in two glioblastomas, both affecting codon 12 of NRAS (c.35G>A, p.G12D). Three additional tumors carried BRAF mutations altering the known hot-spot codon 599 (c.1796T>A, p.V599E). None of these five glioblastomas showed amplification of the EGFR or PDGFRA genes, while three of the tumors, including two with NRAS and one with BRAF mutation, demonstrated PTEN missense mutations or loss of PTEN mRNA expression. Taken together, our data suggest activating mutations in NRAS or BRAF as a molecular alteration that contributes to aberrant Ras signaling in a small fraction of glioblastomas.

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CRRD Object Information
CRRD ID: 13702875
Created: 2018-07-20
Species: All species
Last Modified: 2018-07-20
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.