FPKM: fragments per kilobase of transcript per million mapped reads; KRT1: keratin 1; miRNA: micro-RNA; miscRNA: miscellaneous RNA; Mt rRNA: mitochondrial ribosomal RNA; Mt tRNA: mitochondrial transference RNA; OAZ3: ornithine decarboxylase antizyme 3; ORT: osmotic resistance test; piRNA: Piwi-interacting RNA; PRM1: protamine 1; PTPRC: protein tyrosine phosphatase receptor type C; rRNA: ribosomal RNA; snoRNA: small nucleolar RNA; snRNA: small nuclear RNA; SRR: sperm recovery rate; tRNA: transfer RNA.

e14109 Background: Activating mutation of the KRAS oncogene is an established predictive biomarker for resistance to anti–epidermal growth factor receptor (anti-EGFR) therapies in advanced colorectal cancer (CRC). BRAF, another component of the EGFR-MAPK signal transduction pathway, is also subject to a common activating mutation in CRC. The aim of this report is to present the mutational status of KRAS, BRAF of an Argentinian population of CR tumors. Methods: Tumor blocks were obtained from 85 consenting patients of various public and private hospitals. We analyzed the presence of KRAS point mutations in codons 12 and 13, and the BRAF-V600E from formalin paraffin fixed sections with Polymerase Chain Reaction (PCR) amplification-sequencing. Results: From a total of 85 patients, 46% F and 54% M, with a median age of 64 years (range, 28-85), 72% (61) where found to be wild type, while the other 28% (24) showed the KRAS mutation in the following amino acids: G12V 30% (7), G12D 17% (4), G12C 17% (4), G12S 9% (2), G12A 4% (1), G13D 25% (6). We analyzed in 45 patients the mutational status of BRAF-V600E, 29 patients presented BRAF and KRAS wild type, 12 had a KRAS mutation while the BRAF was wild type, and 4 patients reveled a mutation of BRAF in the presence of a KRAS wild type. Conclusions: The type of mutation observed in this study corresponds to the findings of previous studies, where the most common KRAS mutation detected was G12V in codon 12 followed by G13D in codon 13. A preliminary report based in 146 patients from Argentine (Perazzo F, et al. 2009) revealed marked differences in KRAS mutation rates compared to our findings, showing the following percentage of mutations: G12V 62% vs. 30% , G12D 26% vs. 17% and G13R 1.7% vs. 0%, G13D 0% vs. 25%, respectively. BRAF mutational status was according to international and national reports.

No abstract