EGFR and KRAS Mutations in Lung Parenchyma of Subjects With EGFR/KRAS Wild-Type Lung Adenocarcinoma
Chalela, Roberto (Institut Hospital del Mar d'Investigacions Mèdiques)
González-García, Jose Gregorio (Institut Hospital del Mar d'Investigacions Mèdiques)
Khilzi, Karys (Institut Hospital del Mar d'Investigacions Mèdiques)
Curull Serrano, Víctor (Universitat Autònoma de Barcelona. Departament de Medicina)
Sánchez-Font, Albert (Institut Hospital del Mar d'Investigacions Mèdiques)
Longarón, Raquel (Hospital del Mar (Barcelona, Catalunya))
Rodrigo-Calvo, María Teresa (Hospital del Mar (Barcelona, Catalunya))
Martín-Ontiyuelo, Clara (Institut Hospital del Mar d'Investigacions Mèdiques)
Gea Guiral, Joaquim (Institut Hospital del Mar d'Investigacions Mèdiques)
Bellosillo Paricio, Beatriz (Institut Hospital del Mar d'Investigacions Mèdiques)

Data:	2021
Resum:	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.
Ajuts:	Agència de Gestió d'Ajuts Universitaris i de Recerca 2014/SGR-424 Agència de Gestió d'Ajuts Universitaris i de Recerca 2017/SGR-205
Nota:	Altres ajuts: This study have been funded by Fundació La Marató TV3-201305-30; FUCAP 2015; SEPAR 2015 (Project and; Fellowship).
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Matèria:	Adenocacinoma lung ; Driver mutation ; EGFR-epidermal growth factor receptor ; KRAS ; Prognosis
Publicat a:	Pathology and Oncology Research, Vol. 27 (march 2021) , ISSN 1532-2807

DOI: 10.3389/pore.2021.598292
PMID: 34257550

6 p, 1.0 MB

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