Numerous clinical studies have shown that anti-EGFR therapies are effective only 
in a subset of patients with colorectal cancer. Even though mutations in the 
KRAS gene have been confirmed as negative predictors of the response to 
EGFR-targeted therapies, not all KRAS wild-type (wt-KRAS) patients will respond 
to treatment. Recent studies have demonstrated that additionally wild-type BRAF 
(wt-BRAF) genotype is required for response to panitumumab or cetuximab, 
suggesting that BRAF genotype criteria should be used together with KRAS 
genotype for selecting the patients who are about to benefit from the anti-EGFR 
therapy. In this study, 239 samples obtained from 215 patients with metastatic 
colorectal cancer were tested for the presence of the seven most common 
mutations in the KRAS gene and the V600E mutation in the BRAF gene. Among the 
tested patients, 53.8% of patients had wt-KRAS genotype and 46.2% were KRAS 
mutants. Around five percent (5.1%) of the tested patients bore the V600E 
mutation in BRAF gene. All the patients showing to have the V600E mutation in 
BRAF were wt-KRAS. The concordance of KRAS and BRAF mutational status between 
primary and metastatic tumor tissue samples was 100%. We have shown that the 
proportions of mutated and non-mutated KRAS in Slovene patients, as well as the 
proportion of V600E mutations in BRAF is similar to genotyping results reported 
by other authors. The tested seven KRAS mutations on codons 12 and 13 were 
mutually exclusive with the V600E mutation in the BRAF gene. Summing up the 
results about the KRAS and the BRAF mutation carriers from our study, the 
portion of potentially non-responsive patients for the anti-EGFR treatment is 
51.3%.