RT Journal Article
T1 Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.
A1 Sánchez-Muñoz, Alfonso
A1 Gallego Domínguez, Elena María
A1 Luque, Vanessa de
A1 Pérez-Rivas, Luís G
A1 Vicioso Recio, Luís
A1 Ribelles Entrena, Nuria
A1 Lozano Castro, José
A1 Alba Conejo, Emilio
K1 KRT5 protein, human
K1 EGFR protein, human
K1 ERBB2 protein, human
K1 KRAS protein, human
K1 Análisis Mutacional de ADN
K1 Regulación Neoplásica de la Expresión Génica
K1 Inmunohistoquímica
K1 Queratina-5
K1 Queratina-6
K1 Mutación
K1 Neoplasias vasocelulares
K1 Selección de pacientes
K1 Reacción en Cadena de la Polimerasa
K1 Inhibidores de las Proteína Quinasas
K1 Proteínas Proto-Oncogénicas
K1 Receptor del Factor de Crecimiento Epidérmico
K1 Receptores estrogénicos
K1 Receptores de progesterona
K1 Marcadores biológicos de tumor
K1 Marcadores tumorales
K1 Proteínas ras
K1 Neoplasias de la mama
AB 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.
PB BioMed Central
YR 2010
FD 2010-04-13
LK http://hdl.handle.net/10668/664
UL http://hdl.handle.net/10668/664
LA en
NO Sánchez-Muñoz A, Gallego E, Luque V de, Pérez-Rivas LG, Vicioso L, Ribelles N, et al. Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer. BMC Cancer; 10:136
NO Journal Article; Research Support, Non-U.S. Gov't;
DS RISalud
RD Aug 5, 2025