181P - Prognostic relevance of fibroblast growth factor receptor 1 (FGFR1) gene copy number in pure lung squamous-cell carcinoma

Date 30 September 2012
Event ESMO Congress 2012
Session Poster presentation II
Topics Biomarkers
Lung and other Thoracic Tumours
Presenter Luigi Terracciano
Authors L. Terracciano1, E. Rossi2, L. Landi2, M. Roncalli3, A. D'Incecco2, M. D'Arcangelo2, A. Destro3, M. Incarbone4, M. Andreozzi1, F. Cappuzzo5
  • 1Pathology, University Hospital Basel, CH-4031 - Basel/CH
  • 2Oncology, Istituto Toscano Tumori, Livorno/IT
  • 3Pathology, Milan University-Istituto Clinico Humanitas Cancer center, Rozzano/IT
  • 4Surgery, Thoracic Surgery, Ospedale S.Giuseppe-Multimedica, Milan/IT
  • 5U.o. Oncologia Medica, Istituto Toscano Tumori, Livorno/IT

Abstract

Background

FGFR1 belongs to a family of five different receptors often dysregulated in human malignancies, including lung cancer. Recent studies showed that gene amplification is one of the mechanisms potentially responsible for FGFR dysregulation. Although FGFR1 gene amplification has been reported in up to 20% of lung cancer patients with squamous-cell carcinoma (SCC), prognostic effect is unknown. Aim of the present study was to assess the prognostic role of FGFR1 gene copy number (GCN) in pure lung SCC.

Methods

A total of 378 patients were included in the present study. Pure SCC was defined as a tumor positive for P40 and negative for TTF1 using immunohistochemistry. FGFR1 was evaluated by fluorescence in situ hybridization (FISH) in tissue microarray sections from primary lung tumors. All cases with an FGFR1/centromere ratio ≥ 2 were considered as amplified (FGFR1 FISH+).

Results

Among patients included onto the study, FGFR1 FISH analysis was successfully performed in 304 and 32 (10.5%) were FGFR1 FISH+. FGFR1 amplification was significantly associated with P40 positive status (p = 0.002) and with lack of TTF1 expression (p = 0.005). In the whole population, no difference in disease-free survival (DFS) and overall survival (OS) was detected between FGFR1 FISH positive and negative patients (DFS: 17.2 versus 17.0 months, p = 0.98; OS: not reached in both groups, p = 0.2). In the group of patients p40 + /TTF1 negative (N = 66), 14 (21.2%) displayed FGFR1 gene amplification. No difference in survival was detected between FGFR1 FISH+ and negative patients in p40+ versus p40 negative (OS not reached versus 46.2 months, p = 0.41 in FGFR1 FISH + /p40+ versus any negative), nor in TTF1 negative versus TTF1+ (OS not reached versus 41.8 months in FGFR1 FISH + /TTF1 negative versus other subgroups) nor in FGFR FISH + /p40 + /TTF1 negative versus FGFR negative/p40 + /TTF1 negative (37.3 months versus not reached, p = 0.77).

Conclusions

FGFR1 is amplified in 21% of pure lung SCC with no prognostic effect. The high percentage of gene amplification detected further support anti-FGFR1 strategies in individuals with pure SCC.

Disclosure

All authors have declared no conflicts of interest.