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Article

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

Lung cancer (Amsterdam, Netherlands) - 1 Apr 2013

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

Abstract excerpt

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...

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Share to Adenocarcinoma
Share to Carcinoma, Neuroendocrine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Transformation, Neoplastic

Share to Drug Resistance, Neoplasm

Share to Erlotinib Hydrochloride

Share to Neoplasm Grading

Share to Quinazolines

Share to Small Cell Lung Carcinoma

Source

Identifiers

PMID: 23312887
DOI: 10.1016/j.lungcan.2012.12.019

Genes

EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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