Transformation to "high grade" neuroendocrine carcinoma as an acquired drug resistance mechanism in EGFR-mutant lung adenocarcinoma.
Data(s) |
01/04/2013
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Resumo |
Several different acquired resistance mechanisms of EGFR mutant lung adenocarcinoma to EGFR-tyrosine kinase inhibitor (TKI) therapy have been described, most recently transformation to small cell lung carcinoma (SCLC). We describe the case of a 46-year-old female with relapsed EGFR exon 19 deletion lung adenocarcinoma treated with erlotinib, and on resistance, cisplatin-pemetrexed. Liver rebiopsy identified an afatinib-resistant combined SCLC and non-small cell carcinoma with neuroendocrine morphology, retaining the EGFR exon 19 deletion. This case highlights acquired EGFR-TKI resistance through transformation to the high-grade neuroendocrine carcinoma spectrum and that that such transformation may not be evident at time of progression on TKI therapy. |
Identificador | |
Idioma(s) |
eng |
Direitos |
info:eu-repo/semantics/restrictedAccess |
Fonte |
Popat , S , Wotherspoon , A , Nutting , C M , Gonzalez , D , Nicholson , A G & O'Brien , M 2013 , ' Transformation to "high grade" neuroendocrine carcinoma as an acquired drug resistance mechanism in EGFR-mutant lung adenocarcinoma. ' Lung Cancer , vol 80 , no. 1 , pp. 1-4 . DOI: 10.1016/j.lungcan.2012.12.019 |
Palavras-Chave | #Adenocarcinoma #Carcinoma, Neuroendocrine #Cell Transformation, Neoplastic #Drug Resistance, Neoplasm #Erlotinib Hydrochloride #Female #Humans #Immunohistochemistry #Lung Neoplasms #Middle Aged #Mutation #Neoplasm Grading #Protein Kinase Inhibitors #Quinazolines #Receptor, Epidermal Growth Factor #Small Cell Lung Carcinoma |
Tipo |
article |