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1.
Oncol. clín ; 21(3): 71-73, 2016. ilus
Artigo em Espanhol | LILACS | ID: biblio-882196

RESUMO

La mutación del receptor del factor de crecimiento epidérmico (EGFR) en los tumores de pulmón puede observarse en un 10-47% de pacientes. El 90% de las mutaciones son deleciones del exón 19 o mutaciones puntuales del L858R del exón 21, y se asocian a respuesta con inhibidores de tirosina quinasa (TKI). La mutación predictora de resistencia a TKI más frecuente es la T790M en el cromosoma 20, y puede observarse en un 50% de los pacientes expuestos a TKI (mutación secundaria, principal mecanismo de resistencia a TKI) y en menos del 5% de los pacientes de novo. La presencia de mutación T790M de novo concomitante con mutaciones sensibles (doble mutación) es poco frecuente y se cree que podría expresar menor sensibilidad a los TKI. Se presenta un caso clínico correspondiente a una mujer portadora de una doble mutación (deleción exón 19 y T790M) de novo, que fue tratado con erlotinib en primera línea, presentando respuesta objetiva por 10 meses. En el caso descripto, portador de una doble mutación, la respuesta a erlotinib en primera línea fue similar a la comunicada en pacientes con mutaciones predictoras de respuesta (AU)


EGFR mutation in NSCLC has been reported in 10-47% of patients. 90% of these mutations are deletions in exon 19 or point mutations of L858R in exon 21, and are associated to TKI response. T790M is the most common (50%) emerging mutation after first line TKI therapy, associated with resistance. Although this mutation has been reported before TKI therapy (de novo) its prevalence is less than 5%. Concomitant de novo sensitizing and resistance mutations (double mutation) is extremely unlikely, it could be associated with less sensitivity. We describe a patient with a de novo double mutation (deletion exon 19 and T790M) who was treated with erlotinib in first line with objective response lasting 10 months. Our patient, harboring a double mutation had a response to first line erlotinib lasting the same as the median progression free survival reported in patients with sensitizing mutations (AU)


Assuntos
Humanos , Feminino , Pessoa de Meia-Idade , Adenocarcinoma/diagnóstico , Neoplasias Pulmonares , Mutação/genética , Receptores ErbB , Adenocarcinoma/diagnóstico por imagem
2.
Onco Targets Ther ; 6: 603-8, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23745052

RESUMO

OBJECTIVES: The aim of this paper was to investigate the efficacy and activity variation associated with phosphoinositide 3-kinase (PI3K) signal transduction when combining erlotinib with radiation, using different administration schedules. MATERIALS AND METHODS: Erlotinib was delivered to A973 cancer cells in the following three ways: (1) irradiation after administration, (2) irradiation upon administration, and, (3) irradiation before administration. The cell-survival rates were detected using colony-forming assays, while cell apoptosis was detected with flow cytometry. The expression levels of C-MET, p-C-MET, AKT, and p-AKT were determined via Western blotting analysis, under 6 Gy irradiation with/ without erlotinib. RESULTS: The sensitizer enhancement ratios (SERs) of erlotinib irradiation after administration, irradiation upon administration, and irradiation before administration groups were 2.19, 1.53, and 1.38, respectively. A higher apoptosis rate was observed when irradiation was delivered after erlotinib. In addition, changes in cell apoptosis were found to be related to concurrent changes in C-MET, p-C-MET, AKT, and p-AKT expression. Protein expression increased in the combination groups, with trends showing a negative relationship with cell apoptosis. CONCLUSION: The radiosensitive effect of erlotinib varied because of the different administration schedules; this variation may be related to PI3K signal transduction and its associated regulating effect.

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