Hiroaki Akamatsu1, Akira Ono2, Takehito Shukuya3, Asuka Tsuya4, Yukiko Nakamura5, Hirotsugu Kenmotsu6, Tateaki Naito7, Haruyasu Murakami8, Masahiro Endo9, Takashi Nakajima10, Nobuyuki Yamamoto11, Toshiaki Takahashi12. 1. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan; Third Department of Internal Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan. Electronic address: h-akamat@wakayama-med.ac.jp. 2. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: a.ono@scchr.jp. 3. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan; Department of Respiratory Medicine, Juntendo University, School of Medicine, 2-1-1 Hongou, Bunkyou-ku, Tokyo 113-8421, Japan. Electronic address: tshukuya@juntendo.ac.jp. 4. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan; Department of Clinical Oncology, Osaka City General Hospital, 2-13-22 Miyakojimahondohri, Miyakojima-ku, Osaka 534-0021, Japan. Electronic address: a-tsuya@hospital.city.osaka.jp. 5. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan; Department of Respiratory Medicine, Yokohama Munincipal Citizen׳s Hospital, 56 Okazawa-cho, Hodogaya-ku, Yokohama, Kanagawa 240-8555, Japan. Electronic address: yu43-nakamura@city.yokohama.jp. 6. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: h.kenmotsu@scchr.jp. 7. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: t.naito@scchr.jp. 8. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: ha.murakami@scchr.jp. 9. Division of Diagnostic Radiology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: m.endo@scchr.jp. 10. Division of Radiation Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: t.nakajima@scchr.jp. 11. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan; Third Department of Internal Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-8509, Japan. Electronic address: nb.yamamo@wakayama-med.ac.jp. 12. Division of Thoracic Oncology, Shizuoka Cancer Center, 1007 Shimonagakubo, Nagaizumi-cho Sunto-gun, Shizuoka 411-8777, Japan. Electronic address: t.takahashi@scchr.jp.
Abstract
INTRODUCTION: A recent retrospective analysis found that 23% of non-small cell lung cancer patients who acquired resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) demonstrated "disease flare" after discontinuation of EGFR-TKIs. However, limitations of this study present the need for further investigation to elucidate this phenomenon in more detail. METHODS: We reviewed the clinical records of EGFR mutated patients with advanced lung adenocarcinoma who were treated with gefitinib monotherapy in our hospital between January 2007 and December 2010. Disease flare was defined as unexpected interventions (e.g. radiation therapy or pleural drainage), hospitalization, or death attributable to disease progression after gefitinib discontinuation. RESULTS: Among 52 eligible patients, only two experienced disease flare (4%; 95% confidence interval: 1-13%). In both cases, interval time from gefitinib discontinuation to disease flare was 11 days, and the brain was the site of flare. Survival time after gefitinib was significantly shorter in the flare patients (78 and 97 days, respectively) compared with the no-flare patients (median 388 days). CONCLUSIONS: Our analysis demonstrated a lower incidence rate of disease flare after gefitinib discontinuation compared with the previous report, but the prognosis was similarly poor.
INTRODUCTION: A recent retrospective analysis found that 23% of non-small cell lung cancerpatients who acquired resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) demonstrated "disease flare" after discontinuation of EGFR-TKIs. However, limitations of this study present the need for further investigation to elucidate this phenomenon in more detail. METHODS: We reviewed the clinical records of EGFR mutated patients with advanced lung adenocarcinoma who were treated with gefitinib monotherapy in our hospital between January 2007 and December 2010. Disease flare was defined as unexpected interventions (e.g. radiation therapy or pleural drainage), hospitalization, or death attributable to disease progression after gefitinib discontinuation. RESULTS: Among 52 eligible patients, only two experienced disease flare (4%; 95% confidence interval: 1-13%). In both cases, interval time from gefitinib discontinuation to disease flare was 11 days, and the brain was the site of flare. Survival time after gefitinib was significantly shorter in the flare patients (78 and 97 days, respectively) compared with the no-flare patients (median 388 days). CONCLUSIONS: Our analysis demonstrated a lower incidence rate of disease flare after gefitinib discontinuation compared with the previous report, but the prognosis was similarly poor.