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// Hyo Song Kim 1,* , Seung Eun Lee 2,* , Yoon Sung Bae 3,* , Dae Joon Kim 4 , Chang-Geol Lee 5 , Jin Hur 6 , Hyunsoo Chung 7 , Jun Chul Park 7 , Da Hyun Jung 7 , Sung Kwan Shin 7 , Sang Kil Lee 7 , Yong Chan Lee 7 , Hye Ryun Kim 1 , Yong Wha Moon 1 , Joo Hang Kim 1 , Young Mog Shim 8 , Susan S. Jewell 9 , Hyunki Kim 3 , Yoon-La Choi 2 and Byoung Chul Cho 1 1 Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea 2 Departments of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 3 Department of Pathology, Yonsei University College of Medicine, Seoul, Korea 4 Department of Thoracic and Cardiovascular Surgery, Yonsei University College of Medicine, Seoul, Korea 5 Department of Radiation Oncology, Yonsei University College of Medicine, Seoul, Republic of Korea 6 Department of Radiology, Yonsei University College of Medicine, Seoul, Republic of Korea 7 Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea 8 Department of Thoracic Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 9 Abbott Molecular Laboratories, Des Plaines, IL * These authors contributed equally to this work as co-first authors Correspondence: Byoung Chul Cho, email: // Yoon-La Choi, email: // Hyunki Kim, email: // Keywords : Fibroblast growth factor receptor 1, esophageal squamous cell carcinoma, gene amplification, fluorescent in situ hybridization, prognostic factor Received : September 11, 2014 Accepted : December 09, 2014 Published : December 10, 2014 Abstract To investigate the frequency and the prognostic impact of fibroblast growth factor receptor 1 ( FGFR1 ) gene amplification in 526 curatively resected esophageal squamous cell carcinoma (ESCC). Using fluorescent in situ hybridization, high amplification was defined by an FGFR1 /centromer 8 ratio is ≥ 2.0, or average number of FGFR1 signals/tumor cell nucleus ≥ 6.0, or percentage of tumor cells containing ≥ 15 FGFR1 signals or large cluster in ≥ 10%. Low amplification was defined by ≥ 5 FGFR1 signals in ≥ 50%. FGFR2 and FGFR3 mutations were assessed by direct sequencing in 388 cases and no mutation was detected. High and low amplification were detected in 8.6% and 1.1%, respectively. High FGFR1 amplification had significantly shorter disease-free survival (34.0 vs 158.5 months P =0.019) and overall survival (52.2 vs not reached P =0.022) than low/no amplification group. After adjusting for sex, smoking, stage, histology, and adjuvant treatment, high FGFR1 amplification had a greater risk of recurrence (adjusted hazard ratio [AHR], 1.6; P =0.029) and death (AHR, 1.53; P =0.050). High amplification was significantly higher in current smokers than former and never-smokers ( P trend |
