<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-05T18:06:57Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/29544" metadataPrefix="marc">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/29544</identifier><datestamp>2026-02-03T11:27:03Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37953</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Sánchez-Muñoz, Alfonso</subfield>
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      <subfield code="a">Gallego-Domínguez, Elena María</subfield>
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      <subfield code="a">De Luque, Vanessa</subfield>
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      <subfield code="a">Pérez-Rivas, Luis G.</subfield>
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      <subfield code="a">Vicioso-Recio, Luis Prudencio</subfield>
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      <subfield code="a">Ribelles, Nuria</subfield>
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      <subfield code="a">Lozano-Castro, José</subfield>
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      <subfield code="a">Alba-Conejo, Emilio</subfield>
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      <subfield code="c">2010-04-13</subfield>
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      <subfield code="a">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,&#xd;
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.&#xd;
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&#xd;
(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.&#xd;
Results: We found no evidence of KRAS oncogenic mutations in all analyzed tumors.&#xd;
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&#xd;
about 60% of all cases.</subfield>
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      <subfield code="a">Sánchez-Muñoz A, Gallego E, de Luque V, Pérez-Rivas LG, Vicioso L, Ribelles N, Lozano J, Alba E. Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer. BMC Cancer. 2010 Apr 13;10:136. doi: 10.1186/1471-2407-10-136. PMID: 20385028; PMCID: PMC2868051.</subfield>
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      <subfield code="a">https://hdl.handle.net/10630/29544</subfield>
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      <subfield code="a">10.1186/1471-2407-10-136</subfield>
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      <subfield code="a">Cáncer - Aspectos genéticos</subfield>
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      <subfield code="a">Mamas - Cáncer - Aspectos genéticos</subfield>
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      <subfield code="a">Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.</subfield>
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