Please use this identifier to cite or link to this item: http://hdl.handle.net/10668/664
Title: Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.
Authors: Sánchez-Muñoz, Alfonso
Gallego Domínguez, Elena María
Luque, Vanessa de
Pérez-Rivas, Luís G
Vicioso Recio, Luís
Ribelles Entrena, Nuria
Lozano Castro, José
Alba Conejo, Emilio
metadata.dc.contributor.authoraffiliation: [Sánchez-Muñoz,A; Ribelles Entrena,N; Alba Conejo,E] Servicio de Oncología Médica, Hospital Universitario Virgen de la Victoria, Málaga, España. [Gallego Domínguez,E; Vicioso Recio,L] Servicio de Anatomía Patológica, Hospital Universitario Virgen de la Victoria, Málaga, España. [Sánchez-Muñoz,A; Gallego Domínguez,EM; Luque,V de; Pérez-Rivas,LG; Vicioso Recio,L; Ribelles Entrena,N; Lozano Castro,J; Alba Conejo,E] Laboratorio de Investigación Biomédica (LIB-IMABIS), Hospital Universitario Virgen de la Victoria, Málaga, España. [Lozano Castro,J] Dpto. de Biología Molecular y Bioquímica, Facultad de Ciencias, Universidad de Málaga, España.
Keywords: KRT5 protein, human;EGFR protein, human;ERBB2 protein, human;KRAS protein, human;Análisis Mutacional de ADN;Regulación Neoplásica de la Expresión Génica;Inmunohistoquímica;Queratina-5;Queratina-6;Mutación;Neoplasias vasocelulares;Selección de pacientes;Reacción en Cadena de la Polimerasa;Inhibidores de las Proteína Quinasas;Proteínas Proto-Oncogénicas;Receptor del Factor de Crecimiento Epidérmico;Receptores estrogénicos;Receptores de progesterona;Marcadores biológicos de tumor;Marcadores tumorales;Proteínas ras;Neoplasias de la mama
metadata.dc.subject.mesh: Medical Subject Headings::Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Genetic Techniques::Sequence Analysis::Sequence Analysis, DNA::DNA Mutational Analysis
Medical Subject Headings::Check Tags::Female
Medical Subject Headings::Phenomena and Processes::Genetic Phenomena::Genetic Processes::Gene Expression Regulation::Gene Expression Regulation, Neoplastic
Medical Subject Headings::Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans
Medical Subject Headings::Analytical, Diagnostic and Therapeutic Techniques and Equipment::Diagnosis::Diagnostic Techniques and Procedures::Clinical Laboratory Techniques::Cytological Techniques::Histocytochemistry::Immunohistochemistry
Medical Subject Headings::Chemicals and Drugs::Macromolecular Substances::Polymers::Biopolymers::Intermediate Filament Proteins::Keratins::Keratins, Type II::Keratin-5
Medical Subject Headings::Chemicals and Drugs::Macromolecular Substances::Polymers::Biopolymers::Intermediate Filament Proteins::Keratins::Keratins, Type II::Keratin-6
Medical Subject Headings::Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation
Medical Subject Headings::Diseases::Neoplasms::Neoplasms by Histologic Type::Neoplasms, Glandular and Epithelial::Neoplasms, Basal Cell
Medical Subject Headings::Health Care::Health Services Administration::Patient Care Management::Patient Selection
Medical Subject Headings::Analytical, Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Genetic Techniques::Nucleic Acid Amplification Techniques::Polymerase Chain Reaction
Medical Subject Headings::Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Enzyme Inhibitors::Protein Kinase Inhibitors
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::Neoplasm Proteins::Oncogene Proteins::Proto-Oncogene Proteins
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Transferases::Phosphotransferases::Phosphotransferases (Alcohol Group Acceptor)::Protein Kinases::Protein-Tyrosine Kinases::Receptor Protein-Tyrosine Kinases::Receptor, Epidermal Growth Factor
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Transferases::Phosphotransferases::Phosphotransferases (Alcohol Group Acceptor)::Protein Kinases::Protein-Tyrosine Kinases::Receptor Protein-Tyrosine Kinases::Receptor, erbB-2
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::DNA-Binding Proteins::Receptors, Cytoplasmic and Nuclear::Receptors, Steroid::Receptors, Estrogen
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::DNA-Binding Proteins::Receptors, Cytoplasmic and Nuclear::Receptors, Steroid::Receptors, Progesterone
Medical Subject Headings::Chemicals and Drugs::Biological Factors::Biological Markers::Tumor Markers, Biological
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Acid Anhydride Hydrolases::GTP Phosphohydrolases::GTP-Binding Proteins::Monomeric GTP-Binding Proteins::ras Proteins
Medical Subject Headings::Diseases::Neoplasms::Neoplasms by Site::Breast Neoplasms
Issue Date: 13-Apr-2010
Publisher: BioMed Central
Citation: 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
Abstract: 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.
Description: Journal Article; Research Support, Non-U.S. Gov't;
URI: http://hdl.handle.net/10668/664
metadata.dc.relation.publisherversion: http://www.biomedcentral.com/1471-2407/10/136
metadata.dc.identifier.doi: 10.1186/1471-2407-10-136
ISSN: 1471-2407 (Online)
Appears in Collections:01- Artículos - Hospital Virgen de la Victoria

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