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EGFR and KRAS mutations in lung parenchyma of subjects with EGFR/KRAS wild-type lung adenocarcinoma

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dc.contributor.author Chalela Rengifo, Roberto José, 1985-
dc.contributor.author González-García, José Gregorio
dc.contributor.author Khilzi, Karys
dc.contributor.author Curull Serrano, Víctor
dc.contributor.author Sánchez Font, Albert
dc.contributor.author Longarón Rozalen, Raquel
dc.contributor.author Rodrigo Calvo, Maria Teresa
dc.contributor.author Martín-Ontiyuelo, Clara
dc.contributor.author Gea Guiral, Joaquim
dc.contributor.author Bellosillo Paricio, Beatriz
dc.date.accessioned 2021-10-06T06:57:11Z
dc.date.available 2021-10-06T06:57:11Z
dc.date.issued 2021
dc.identifier.citation Chalela R, González-García JG, Khilzi K, Curull V, Sánchez-Font A, Longarón R, Rodrigo-Calvo MT, Martín-Ontiyuelo C, Gea J, Bellosillo B. EGFR and KRAS mutations in lung parenchyma of subjects with EGFR/KRAS wild-type lung adenocarcinoma. Pathol Oncol Res. 2021;27:598292. DOI: 10.3389/pore.2021.598292
dc.identifier.issn 1219-4956
dc.identifier.uri http://hdl.handle.net/10230/48576
dc.description.abstract The acquisition of driver mutations in non-tumoral cells appears to be very important during the carcinogenesis of adenocarcinoma (ADC). Recent studies suggest that cancer-related mutations may not necessarily be present only in malignant cells, but also in histologically "healthy cells". Objective: to demonstrate the presence of EGFR or KRAS mutations in non-tumoral lung cells in subjects with ADC and negative mutational status. Results: mutations in EGFR or KRAS oncogenes were identified in the normal lung in 9.7% of the subjects. Exon 21 substitution L858R in EGFR was detected in two cases while the exon 19 deletion E746-A750 in the EGFR, the G12C and G12D substitutions in the KRAS were detected once. One patient presented three different mutations in the normal lung parenchyma (EGFR_L858R, KRAS_G12C and KRAS_G12D). The negative-mutation status of the tumor and the mutations detected in the "normal lung" were confirmed using highly sensitive and specific TaqMan PCR (CAST-PCR). No differences were found in terms of progression, progression-free survival or overall survival during the 18 months follow-up. Conclusions: These results confirm the presence of driver mutations in the histologically normal lung parenchyma cells in the absence of mutations coexisting with the primary tumor.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Frontiers
dc.relation.ispartof Pathol Oncol Res. 2021;27:598292
dc.rights © 2021 Chalela, González-García, Khilzi, Curull, Sánchez-Font, Longarón, Rodrigo-Calvo, Martín-Ontiyuelo, Gea and Bellosillo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.title EGFR and KRAS mutations in lung parenchyma of subjects with EGFR/KRAS wild-type lung adenocarcinoma
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.3389/pore.2021.598292
dc.subject.keyword EGFR–epidermal growth factor receptor
dc.subject.keyword KRAS
dc.subject.keyword Prognosis
dc.subject.keyword Adenocacinoma lung
dc.subject.keyword Driver mutation
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion

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