Histological transformation of ALK rearranged adenocarcinoma into small cell lung cancer: A new mechanism of resistance to ALK inhibitors. (December 2016)

• Record Type: Journal Article
• Authors: Levacq, Delphine; D'Haene, Nicky; de Wind, Roland; Remmelink, Myriam; Berghmans, Thierry
• Is Part Of: Lung cancer. Volume 102(2016)
• Page Start: 38
• Page End: 41
• Publication Date: 2016-12
• Subjects: ALK translocation -- Lung neoplasms -- Small cell cancer transformation; Lungs -- Cancer -- Periodicals; Lung Neoplasms -- Abstracts; Lung Neoplasms -- Periodicals; Poumons -- Cancer -- Périodiques; Lungs -- Cancer; Periodicals; Electronic journals; Electronic journals; 616.99424
• DOI: 10.1016/j.lungcan.2016.10.012
• Languages: English
• ISSNs: 0169-5002

Abstract

Highlights: Resistance to ALK tyrosine kinase inhibitors is common. Main resistances: gatekeeper mutation, bypass signaling, ALK amplification. ALK translocation is exceptional in primitive SCLC. SCLC transformation is a known resistance mechanism to EGFR TKI. SCLC transformation is uncommon in ALK rearranged adenocarcinoma. Abstract: Various mechanisms of resistance to ALK inhibitors in ALK rearranged adenocarcinomas are reported including secondary gatekeeper mutations, bypass signaling or ALK amplifications as the commonest ones. We report a new mechanism of resistance with transformation of adenocarcinoma into small cell lung cancer. A 53-year-old non-smoker woman, experienced cancer progression after two lines of ALK inhibitors. A new biopsy showed a small cell lung cancer. FISH revealed persistent ALK rearrangement with an atypical pattern and complete loss of the 5′ region of the ALK gene.