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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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Survival analysis on the basis of FGFR1 amplification (high, low, and no amplification)(A) Median DFS was 34.0 months in the high FGFR1 amplification group, not reached in low amplification group, and 158.5 months in the no amplification group. (B) The median OS was 52.2 months in the high FGFR1 amplification group, and 72.0 months in the low amplification group, and not reached in the no amplification group.
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Figure 2: Survival analysis on the basis of FGFR1 amplification (high, low, and no amplification)(A) Median DFS was 34.0 months in the high FGFR1 amplification group, not reached in low amplification group, and 158.5 months in the no amplification group. (B) The median OS was 52.2 months in the high FGFR1 amplification group, and 72.0 months in the low amplification group, and not reached in the no amplification group.

Mentions: The median DFS for each of the three FGFR groups was 34.0 months in the high FGFR1 amplification, not reached (NR) in low amplification group, and 158.5 months in the no amplification group (Figure 2A). By using pair-wise comparison, patients with high FGFR1 amplification showed a significantly shorter DFS than those with no amplification (34.0 vs 158.5 months in no amplification, P=0.020). The median DFS of high amplification and low amplification were not significantly different (34.0 vs NR in low amplification, P=0.272), probably due to small sample size in the low amplification group. The median DFS was similar between low amplification and no amplification group in pair-wise comparison (P=0.639). The median OS for each of the three FGFR groups was 52.2 months in the high FGFR1 amplification, 72.0 months in the low amplification, and not reached in the no amplification (Figure 2B). By using pair-wise comparison, patients with high FGFR1 amplification showed a significantly shorter OS than those with no amplification (52.2 vs NR in no amplification, P=0.021). The OS times of high amplification and low amplification were not significantly different (52.2 vs 72.0 in low amplification, P=0.637), probably due to small sample size in the low amplification group. The median OS was similar between low amplification and no amplification group in pair-wise comparison (P=0.517).


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)

Survival analysis on the basis of FGFR1 amplification (high, low, and no amplification)(A) Median DFS was 34.0 months in the high FGFR1 amplification group, not reached in low amplification group, and 158.5 months in the no amplification group. (B) The median OS was 52.2 months in the high FGFR1 amplification group, and 72.0 months in the low amplification group, and not reached in the no amplification group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Survival analysis on the basis of FGFR1 amplification (high, low, and no amplification)(A) Median DFS was 34.0 months in the high FGFR1 amplification group, not reached in low amplification group, and 158.5 months in the no amplification group. (B) The median OS was 52.2 months in the high FGFR1 amplification group, and 72.0 months in the low amplification group, and not reached in the no amplification group.
Mentions: The median DFS for each of the three FGFR groups was 34.0 months in the high FGFR1 amplification, not reached (NR) in low amplification group, and 158.5 months in the no amplification group (Figure 2A). By using pair-wise comparison, patients with high FGFR1 amplification showed a significantly shorter DFS than those with no amplification (34.0 vs 158.5 months in no amplification, P=0.020). The median DFS of high amplification and low amplification were not significantly different (34.0 vs NR in low amplification, P=0.272), probably due to small sample size in the low amplification group. The median DFS was similar between low amplification and no amplification group in pair-wise comparison (P=0.639). The median OS for each of the three FGFR groups was 52.2 months in the high FGFR1 amplification, 72.0 months in the low amplification, and not reached in the no amplification (Figure 2B). By using pair-wise comparison, patients with high FGFR1 amplification showed a significantly shorter OS than those with no amplification (52.2 vs NR in no amplification, P=0.021). The OS times of high amplification and low amplification were not significantly different (52.2 vs 72.0 in low amplification, P=0.637), probably due to small sample size in the low amplification group. The median OS was similar between low amplification and no amplification group in pair-wise comparison (P=0.517).

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