title: Successful rechallenge with erlotinib in a patient with EGFR-mutant lung adenocarcinoma who developed gefitinib-related interstitial lung disease.
abstract: Small-molecule tyrosine kinase inhibitors (TKIs) targeting the epidermal growth factor receptor (EGFR) pathways are used clinically for patients with non-small cell lung cancer (NSCLC). It is well established that somatic mutations in the kinase domain of the EGFR (Lynch et al. in N Engl J Med 350:2129-2139, 2004; Paez et al. in Science 304:1497-1500, 2004) are strongly associated with the tumor response and clinical outcomes in patients with NSCLC receiving EGFR-TKIs (Mitsudomi and Yatabe in Cancer Sci 98:1817-1824, 2007). Although the most common adverse events are skin rash and diarrhea, the most serious adverse effect reported is drug-related interstitial lung disease (ILD) (Inoue et al. in Lancet 361:137-139, 2003; Ando et al. in J Clin Oncol 24:2549-2556, 2006). The precise mechanism underlying the development of drug-related ILD remains unknown. Here, we describe a case of EGFR-mutant NSCLC who was rechallenged with the small-molecule EGFR antagonist erlotinib after developing gefitinib-related ILD.
authors.affiliation: Department of Respiratory Medicine, School of Medicine, Kitasato University, Kitasato 1-15-1, Sagamihara, Kanagawa 228-8555, Japan. tofukui@med.kitasato-u.ac.jp
authors.forename: Tomoya
authors.initials: T
authors.lastname: Fukui
authors.forename: Sakiko
authors.initials: S
authors.lastname: Otani
authors.forename: Ryuji
authors.initials: R
authors.lastname: Hataishi
authors.forename: Shi-Xu
authors.initials: SX
authors.lastname: Jiang
authors.forename: Yasuto
authors.initials: Y
authors.lastname: Nishii
authors.forename: Satoshi
authors.initials: S
authors.lastname: Igawa
authors.forename: Hisashi
authors.initials: H
authors.lastname: Mitsufuji
authors.forename: Masaru
authors.initials: M
authors.lastname: Kubota
authors.forename: Masato
authors.initials: M
authors.lastname: Katagiri
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Masuda
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy* / Q000235:genetics; D000328:Adult; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000235:genetics*; D000069347:Erlotinib Hydrochloride; D005260:Female; D000077156:Gefitinib; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000139:chemically induced / Q000188:drug therapy*; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics; D009154:Mutation; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D011799:Quinazolines / Q000009:adverse effects / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D047428:Protein Kinase Inhibitors; D011799:Quinazolines; D000069347:Erlotinib Hydrochloride; D066246:ErbB Receptors; D000077156:Gefitinib