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Simultaneous amplification and mutation of KRAS: a therapeutic target in a rare subgroup of glioblastoma?

ABSTRACT: We describe the case of a glioblostoma multiform in a 66 year old female patient showing both amplification and mutation (exon 3; codon 61) of KRAS.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73199 | GEO | 2015/09/19

SECONDARY ACCESSION(S): PRJNA296360

REPOSITORIES: GEO

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Simultaneous amplification and mutation of KRAS: a therapeutic target in a rare subgroup of glioblastoma?

Project description:We describe the case of a glioblostoma multiform in a 66 year old female patient showing both amplification and mutation (exon 3; codon 61) of KRAS. sample was analysed by arrayCGH method using Agilent recommendations. Sample was labeled in Cy5 and co-hybridized with control DNA cy3 labeled.

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Project description:To test whether the addition of a peptide nucleic acid (PNA) clamp, which binds WT KRAS at codon 12, can increase the efficacy of mutation detection for KRASG12D within a targeted NGS setting. We tested the effect of clamping the wild-type KRAS sequence in a reference standard (Tru-Q 7, 1.3% Tier from Horizon Diagnostics, Cambridge, UK) with a KRAS c.35G>A mutation (KRASG12D) at an allelic frequency (AF) of 1.3% assessed by digital droplet PCR (ddPCR). We then re-tested the PNA on circulating-free DNA from a patient harbouring a KRASG12D mutation (at an AF of 3.2%, determined by ddPCR). Multiple runs were conducted using 10, 5, 2.5 and 1ng of DNA input.

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Project description:Mutations of the proto-oncogene KRas, together with the inactivation of the onco-suppressor genes APC and TP53, are considered to have an important role both in the carcinogenesis and in the colorectal tumor progression. The oncogene K-ras has activating mutations, especially in codon 12, in about 40% to 50% of colorectal carcinomas (Andreyev et al., 1998). The mechanism by which oncogenic K-ras alone contribuites to tumor progression in colon cancer is largely unknown. To this end, we have developed a model system where the colorectal adenocarcinoma cell line Colo741 has been stably trasfected with the Kras-G12V or Kras-G12D mutated oncogenes. Our results demonstrate how expression profiling data can be used to interpret changes in cellular characteristics induced by transfection and hence provide some clues as to the mechanisms by which different activated K-Ras impair processes mediated by endogenous wild-type KRas proteins. We made for the production of cell clones that could be utilized as useful in vitro models. The adenocarcinoma cell line Colo741 has been chosen to produce stable transfectants for two mutant forms of KRas2 (Gly12Val and Gly12Asp) and the wild-type coding sequence (as experiment control). After the transfection, the cells have been selected (with G418), cloned (by limited dilutions) and screened (by RT-PCR). The total RNAs, Dnase-treated, from five cell clones per condition, have been pooled. The samples, constituted by biotin-labeled cRNA, derived from a pool of five cell clones obtained from transfection of the adenocarcinoma cell line Colo741 with either pcDNA3.1-KRas2(Wt) or pcDNA3.1-KRas2(Gly12Val) or pcDNA3.1KRas2(Gly12Asp). They were hybridized to a Human Gene 1.0 ST array (Affymetrix). Two technical replicates have been performed for each condition.

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