Activating K-Ras mutations outwith 'hotspot' codons in sporadic colorectal tumours - implications for personalised cancer medicine.
作者： G Smith , R Bounds , H Wolf , R J C Steele , F A Carey
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摘要: Response to EGFR-targeted therapies in colorectal cancer patients has been convincingly associated with Kirsten-Ras (K-Ras) mutation status. Current mandatory testing for patient selection is limited the K-Ras ‘hotspot’ codons 12 and 13. Colorectal tumours (n=106) were screened additional mutations, phenotypes compared transformation Ras GTPase activating assays gene pathway changes induced by individual mutants identified microarray analysis. Taqman-based copy number FISH analyses used investigate amplification. Four mutations (Leu19Phe (1 out of 106 tumours), Lys117Asn 106), Ala146Thr (7 106) Arg164Gln 106)) identified. had similar hotspot whereas Leu19Phe an attenuated phenotype was phenotypically equivalent wt K-Ras. We additionally a new amplification event, present approximately 2% tumours. The identification outwith previously described increases burden one-third. Future screening facilitate optimal treatment should therefore be extended codon 146, addition consider unique molecular signatures mutations.
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