• Tomoya Fukui, Sakiko Otani, Ryuji Hataishi, Shi-Xu Jiang, Yasuto Nishii, Satoshi Igawa, Hisashi Mitsufuji, Masaru Kubota, Masato Katagiri, and Noriyuki Masuda.
• Department of Respiratory Medicine, School of Medicine, Kitasato University, Kitasato 1-15-1, Sagamihara, Kanagawa 228-8555, Japan. tofukui@med.kitasato-u.ac.jp
• Cancer Chemother. Pharmacol. 2010 Mar 1;65(4):803-6.

AbstractSmall-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.

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