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Fibroblast growth factor receptor 1 gene amplification is associated with poor survival in patients with resected esophageal squamous cell carcinoma.
Oncotarget. 2015 Feb 10; 6(4):2562-72.O

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 (Ptrend<0.001) and increased proportional to smoking dosage. High FGFR1 amplification is a frequent oncogenic alteration and an independent poor prognostic factor in resected ESCC.

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Publisher Full Text
ncbi.nlm.nih.gov
impactjournals.com
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Authors+Show Affiliations

Kim HS
Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Lee SE
Departments of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Bae YS
Department of Pathology, Yonsei University College of Medicine, Seoul, Korea.
Kim DJ
Department of Thoracic and Cardiovascular Surgery, Yonsei University College of Medicine, Seoul, Korea.
Lee CG
Department of Radiation Oncology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Hur J
Department of Radiology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Chung H
Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Park JC
Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Jung DH
Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Shin SK
Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Lee SK
Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Lee YC
Division of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Kim HR
Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Moon YW
Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Kim JH
Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Shim YM
Department of Thoracic Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Jewell SS
Abbott Molecular Laboratories, Des Plaines, IL.
Kim H
Department of Pathology, Yonsei University College of Medicine, Seoul, Korea.
Choi YL
Departments of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Cho BC
Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.

MeSH

AdultAgedAged, 80 and overCarcinoma, Squamous CellDisease-Free SurvivalEsophageal NeoplasmsFemaleGene AmplificationHumansIn Situ Hybridization, FluorescenceKaplan-Meier EstimateMaleMiddle AgedNeoplasm Recurrence, LocalPrognosisReceptor, Fibroblast Growth Factor, Type 1Risk FactorsSmoking

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25537505

Citation

Kim, Hyo Song, et al. "Fibroblast Growth Factor Receptor 1 Gene Amplification Is Associated With Poor Survival in Patients With Resected Esophageal Squamous Cell Carcinoma." Oncotarget, vol. 6, no. 4, 2015, pp. 2562-72.
Kim HS, Lee SE, Bae YS, et al. Fibroblast growth factor receptor 1 gene amplification is associated with poor survival in patients with resected esophageal squamous cell carcinoma. Oncotarget. 2015;6(4):2562-72.
Kim, H. S., Lee, S. E., Bae, Y. S., Kim, D. J., Lee, C. G., Hur, J., Chung, H., Park, J. C., Jung, D. H., Shin, S. K., Lee, S. K., Lee, Y. C., Kim, H. R., Moon, Y. W., Kim, J. H., Shim, Y. M., Jewell, S. S., Kim, H., Choi, Y. L., & Cho, B. C. (2015). Fibroblast growth factor receptor 1 gene amplification is associated with poor survival in patients with resected esophageal squamous cell carcinoma. Oncotarget, 6(4), 2562-72.
Kim HS, et al. Fibroblast Growth Factor Receptor 1 Gene Amplification Is Associated With Poor Survival in Patients With Resected Esophageal Squamous Cell Carcinoma. Oncotarget. 2015 Feb 10;6(4):2562-72. PubMed PMID: 25537505.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibroblast growth factor receptor 1 gene amplification is associated with poor survival in patients with resected esophageal squamous cell carcinoma. AU - Kim,Hyo Song, AU - Lee,Seung Eun, AU - Bae,Yoon Sung, AU - Kim,Dae Joon, AU - Lee,Chang-Geol, AU - Hur,Jin, AU - Chung,Hyunsoo, AU - Park,Jun Chul, AU - Jung,Da Hyun, AU - Shin,Sung Kwan, AU - Lee,Sang Kil, AU - Lee,Yong Chan, AU - Kim,Hye Ryun, AU - Moon,Yong Wha, AU - Kim,Joo Hang, AU - Shim,Young Mog, AU - Jewell,Susan S, AU - Kim,Hyunki, AU - Choi,Yoon-La, AU - Cho,Byoung Chul, PY - 2015/09/11/received PY - 2015/12/09/accepted PY - 2014/12/25/entrez PY - 2014/12/30/pubmed PY - 2016/1/16/medline SP - 2562 EP - 72 JF - Oncotarget JO - Oncotarget VL - 6 IS - 4 N2 - 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 (Ptrend<0.001) and increased proportional to smoking dosage. High FGFR1 amplification is a frequent oncogenic alteration and an independent poor prognostic factor in resected ESCC. SN - 1949-2553 UR - https://www.unboundmedicine.com/medline/citation/25537505/Fibroblast_growth_factor_receptor_1_gene_amplification_is_associated_with_poor_survival_in_patients_with_resected_esophageal_squamous_cell_carcinoma_ L2 - http://www.impactjournals.com/oncotarget/misc/linkedout.php?pii=2944 DB - PRIME DP - Unbound Medicine ER -