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Fibroblast growth factor receptor 1 gene amplification is associated with poor survival in patients with resected esophageal squamous cell carcinoma.

Kim HS, Lee SE, Bae YS, Kim DJ, Lee CG, Hur J, Chung H, Park JC, Jung da H, Shin SK, Lee SK, Lee YC, Kim HR, Moon YW, Kim JH, Shim YM, Jewell SS, Kim H, Choi YL, Cho BC - Oncotarget (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.

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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Related in: MedlinePlus

Association of smoking status and high FGFR1 amplification(A) Proportions of high FGFR1 amplification according to never-, former, and current smokers (B) Incidence of high FGFR1 amplification according to smoking dosage.
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Figure 4: Association of smoking status and high FGFR1 amplification(A) Proportions of high FGFR1 amplification according to never-, former, and current smokers (B) Incidence of high FGFR1 amplification according to smoking dosage.

Mentions: As shown in Figure 4A, the incidence of high-level FGFR1 amplification was significantly higher in current smokers than former or never-smokers (Ptrend <0.001). The incidences of high-level FGFR1 amplification in current, former and never-smokers were 19.0%, 2.5%, and 0.8%, respectively. With increment of total cigarette smoking dosage, the incidence of high-level FGFR1 amplification was significantly increased (Figure 4B, Ptrend = 0.001). High-level FGFR1 amplification were 0.8% for never-smokers, 5.8% in patients with 1-10 pack-years, 7.4% with 11-20 pack-years, 9.6% with 21-50 pack-years, and 19.3% with more than 50 pack-years.


Fibroblast growth factor receptor 1 gene amplification is associated with poor survival in patients with resected esophageal squamous cell carcinoma.

Kim HS, Lee SE, Bae YS, Kim DJ, Lee CG, Hur J, Chung H, Park JC, Jung da H, Shin SK, Lee SK, Lee YC, Kim HR, Moon YW, Kim JH, Shim YM, Jewell SS, Kim H, Choi YL, Cho BC - Oncotarget (2015)

Association of smoking status and high FGFR1 amplification(A) Proportions of high FGFR1 amplification according to never-, former, and current smokers (B) Incidence of high FGFR1 amplification according to smoking dosage.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4385871&req=5

Figure 4: Association of smoking status and high FGFR1 amplification(A) Proportions of high FGFR1 amplification according to never-, former, and current smokers (B) Incidence of high FGFR1 amplification according to smoking dosage.
Mentions: As shown in Figure 4A, the incidence of high-level FGFR1 amplification was significantly higher in current smokers than former or never-smokers (Ptrend <0.001). The incidences of high-level FGFR1 amplification in current, former and never-smokers were 19.0%, 2.5%, and 0.8%, respectively. With increment of total cigarette smoking dosage, the incidence of high-level FGFR1 amplification was significantly increased (Figure 4B, Ptrend = 0.001). High-level FGFR1 amplification were 0.8% for never-smokers, 5.8% in patients with 1-10 pack-years, 7.4% with 11-20 pack-years, 9.6% with 21-50 pack-years, and 19.3% with more than 50 pack-years.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.

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.

Show MeSH
Related in: MedlinePlus