Title: RAS mutations distribution in a 108 patients series of colorectal cancer
Abstract: Background As described previously in high impact studies,1 patients with other activating RAS out of codon 2 of kras mutations may also be negative predictive biomarkers for anti-EGFR therapy. Here we present the description of a new series in which has been performed the analysis of mutations in KRAS and NRAS genes. Methods Samples of 108 patients with colorectal cancer were used. DNA were extracted from formalin fixed paraffin embedded samples using COBAS DNA sample preparation kit (Roche). Mutation status was determined by targeted pyrosequencing with N/K RAS Pyro Kit (Qiagen). Results Sixty-four out of 108 samples were wild type (WT) both for KRAS and NRAS. Thirty-five patients presented mutation on KRAS (27 in codon 12, 4 in 13, 1 in 117, and 3 in 146). The rest of the patients (9) presented alterations in NRAS (1 in codon 12, 3 in 13, and 5 in 61). Conclusion Our results closely resemble those published to date,2 but due to small sample size are not fully comparable. Further studies must be done to determine the real distribution of the new RAS mutations. As described previously in high impact studies,1 patients with other activating RAS out of codon 2 of kras mutations may also be negative predictive biomarkers for anti-EGFR therapy. Here we present the description of a new series in which has been performed the analysis of mutations in KRAS and NRAS genes. Samples of 108 patients with colorectal cancer were used. DNA were extracted from formalin fixed paraffin embedded samples using COBAS DNA sample preparation kit (Roche). Mutation status was determined by targeted pyrosequencing with N/K RAS Pyro Kit (Qiagen). Sixty-four out of 108 samples were wild type (WT) both for KRAS and NRAS. Thirty-five patients presented mutation on KRAS (27 in codon 12, 4 in 13, 1 in 117, and 3 in 146). The rest of the patients (9) presented alterations in NRAS (1 in codon 12, 3 in 13, and 5 in 61). Our results closely resemble those published to date,2 but due to small sample size are not fully comparable. Further studies must be done to determine the real distribution of the new RAS mutations.
Publication Year: 2014
Publication Date: 2014-01-01
Language: en
Type: article
Indexed In: ['crossref']
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