%0 Journal Article %A Sánchez-Muñoz, Alfonso %A Gallego Domínguez, Elena María %A Luque, Vanessa de %A Pérez-Rivas, Luís G %A Vicioso Recio, Luís %A Ribelles Entrena, Nuria %A Lozano Castro, José %A Alba Conejo, Emilio %T Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer. %D 2010 %U http://hdl.handle.net/10668/664 %X BACKGROUNDMutational 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.METHODSTotal, 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.RESULTSWe found no evidence of KRAS oncogenic mutations in all analyzed tumors.CONCLUSIONSThis 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. %K KRT5 protein, human %K EGFR protein, human %K ERBB2 protein, human %K KRAS protein, human %K Análisis Mutacional de ADN %K Regulación Neoplásica de la Expresión Génica %K Inmunohistoquímica %K Queratina-5 %K Queratina-6 %K Mutación %K Neoplasias vasocelulares %K Selección de pacientes %K Reacción en Cadena de la Polimerasa %K Inhibidores de las Proteína Quinasas %K Proteínas Proto-Oncogénicas %K Receptor del Factor de Crecimiento Epidérmico %K Receptores estrogénicos %K Receptores de progesterona %K Marcadores biológicos de tumor %K Marcadores tumorales %K Proteínas ras %K Neoplasias de la mama %~