Abstract
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.
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Publication types
-
Case Reports
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenocarcinoma / genetics
-
Adenocarcinoma / metabolism*
-
Adenocarcinoma / pathology
-
Carcinoma, Neuroendocrine / genetics
-
Carcinoma, Neuroendocrine / metabolism*
-
Carcinoma, Neuroendocrine / pathology
-
Cell Transformation, Neoplastic / drug effects
-
Cell Transformation, Neoplastic / genetics
-
Drug Resistance, Neoplasm / drug effects
-
Drug Resistance, Neoplasm / genetics
-
ErbB Receptors / antagonists & inhibitors
-
ErbB Receptors / genetics
-
ErbB Receptors / metabolism*
-
Erlotinib Hydrochloride
-
Female
-
Humans
-
Immunohistochemistry
-
Lung Neoplasms / genetics
-
Lung Neoplasms / metabolism*
-
Lung Neoplasms / pathology
-
Middle Aged
-
Mutation
-
Neoplasm Grading
-
Protein Kinase Inhibitors / therapeutic use
-
Quinazolines / therapeutic use
-
Small Cell Lung Carcinoma / genetics
-
Small Cell Lung Carcinoma / metabolism*
-
Small Cell Lung Carcinoma / pathology
Substances
-
Protein Kinase Inhibitors
-
Quinazolines
-
Erlotinib Hydrochloride
-
ErbB Receptors