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

S. Popat, A. Wotherspoon, C.M. Nutting, D. Gonzalez, A.G. Nicholson, M. O'Brien

Research output: Contribution to journalArticle

59 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)1-4
Number of pages4
JournalLung Cancer
Volume80
Issue number1
DOIs
Publication statusPublished - Apr 2013

Keywords

  • 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

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