BACKGROUND: Mutational analysis of the KRAS gene has recently been established 
as a complementary in vitro diagnostic tool for the identification of patients 
with colorectal cancer who will not benefit from anti-epidermal growth factor 
receptor (EGFR) therapies. Assessment of the mutation status of KRAS might also 
be of potential relevance in other EGFR-overexpressing tumors, such as those 
occurring in breast cancer. Although KRAS is mutated in only a minor fraction of 
breast tumors (5%), about 60% of the basal-like subtype express EGFR and, 
therefore could be targeted by EGFR inhibitors. We aimed to study the mutation 
frequency of KRAS in that subtype of breast tumors to provide a molecular basis 
for the evaluation of anti-EGFR therapies.
METHODS: Total, genomic DNA was obtained from a group of 35 formalin-fixed 
paraffin-embedded, triple-negative breast tumor samples. Among these, 77.1% 
(27/35) were defined as basal-like by immunostaining specific for the 
established surrogate markers cytokeratin (CK) 5/6 and/or EGFR. KRAS mutational 
status was determined in the purified DNA samples by Real Time (RT)-PCR using 
primers specific for the detection of wild-type KRAS or the following seven 
oncogenic somatic mutations: Gly12Ala, Gly12Asp, Gly12Arg, Gly12Cys, Gly12Ser, 
Gly12Val and Gly13Asp.
RESULTS: We found no evidence of KRAS oncogenic mutations in all analyzed 
tumors.
CONCLUSIONS: This study indicates that KRAS mutations are very infrequent in 
triple-negative breast tumors and that EGFR inhibitors may be of potential 
benefit in the treatment of basal-like breast tumors, which overexpress EGFR in 
about 60% of all cases.