Transformation to "high grade" neuroendocrine carcinoma as an acquired drug resistance mechanism in EGFR-mutant lung adenocarcinoma.

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.

• Authors: S Popat, A Wotherspoon, C M Nutting, D Gonzalez, A G Nicholson, M O'Brien
• Journal: Lung cancer (Amsterdam, Netherlands) (Lung Cancer) Vol. 80 Issue 1 Pg. 1-4 (Apr 2013) ISSN: 1872-8332 [Electronic] Ireland
• PMID: 23312887 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

Chemical References

• Protein Kinase Inhibitors
• Quinazolines
• Erlotinib Hydrochloride
• ErbB Receptors

Topics

• Adenocarcinoma (genetics, metabolism, pathology)
• Carcinoma, Neuroendocrine (genetics, metabolism, pathology)
• Cell Transformation, Neoplastic (drug effects, genetics)
• Drug Resistance, Neoplasm (drug effects, genetics)
• ErbB Receptors (antagonists & inhibitors, genetics, metabolism)
• Erlotinib Hydrochloride
• Female
• Humans
• Immunohistochemistry
• Lung Neoplasms (genetics, metabolism, pathology)
• Middle Aged
• Mutation
• Neoplasm Grading
• Protein Kinase Inhibitors (therapeutic use)
• Quinazolines (therapeutic use)
• Small Cell Lung Carcinoma (genetics, metabolism, pathology)