Open AccessEntrectinib for ROS1 ‐rearranged non‐small cell lung cancer after crizotinib‐induced interstitial lung disease: A case report
Author(s) -
Tanimura Mai,
Kataoka Nobutaka,
Kunimatsu Yusuke,
Tsutsumi Rei,
Sato Izumi,
Nakano Takayuki,
Tanimura Keiko,
Takeda Takayuki
Publication year - 2021
Publication title -
respirology case reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.304
H-Index - 9
ISSN - 2051-3380
DOI - 10.1002/rcr2.857
Subject(s) - crizotinib , ros1 , medicine , lung cancer , cancer research , interstitial lung disease , alk inhibitor , c met , oncology , cancer , lung , adenocarcinoma , receptor , hepatocyte growth factor , malignant pleural effusion
Chromosomal rearrangements involving the c‐ros oncogene 1 ( ROS1 ) are identified in approximately 1% of non‐small cell lung cancer (NSCLC) patients. Crizotinib is the first tyrosine kinase inhibitor (TKI) against ROS1 ‐rearranged NSCLC. G2032R, a secondary resistant mutation, is observed in 41% of patients treated with crizotinib. Entrectinib, a TKI against neurotrophic tropomyosin receptor kinase, is reportedly efficacious against ROS1 ‐rearranged NSCLC. However, ROS1 ‐G2032R is resistant to entrectinib both in vitro and in vivo. We report an 85‐year‐old female patient with ROS1 ‐rearranged NSCLC, who developed drug‐induced interstitial lung disease (DI‐ILD) 2 months after crizotinib treatment, and was treated with prednisolone followed by entrectinib. Entrectinib treatment resulted in stable disease with a marginal response after a partial response to crizotinib. Entrectinib treatment following crizotinib cessation due to DI‐ILD was efficacious, which suggested that ROS1 ‐G2032R gatekeeper mutation, frequently observed in crizotinib‐resistant disease, was absent.