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Poster Display

2344 - Targeting FGF2 expression against chemoresistance in colorectal cancer (CRC) cell lines - a potential prognostic biomarker in patients with metastatic colorectal cancer (mCRC) treated with FUFIRI or mIrOx (FIRE1)

Date

08 Oct 2016

Session

Poster Display

Presenters

Arndt Stahler

Citation

Annals of Oncology (2016) 27 (6): 149-206. 10.1093/annonc/mdw370

Authors

A. Stahler1, S. Stintzing2, M. Urbischek3, D.P. Modest2, L. Fischer von Weikersthal4, J. Kumbrink3, V. Heinemann2, T. Kirchner3, A. Jung3

Author affiliations

  • 1 Institute Of Pathology, Klinikum der Universität München, 80337 - München/DE
  • 2 Medical Dept. Iii, Klinikum der Universität München, München/DE
  • 3 Institute Of Pathology, Klinikum der Universität München, München/DE
  • 4 Oncology, Klinikum St. Marien Amberg, Amberg/DE
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Resources

Abstract 2344

Background

Our aim was to evaluate fibroblast growth factor 2 (FGF2) expression in cultivated CRC cell lines exposed to 5-fluorouracil (5-FU) and validate results with clinical data from mCRC patients receiving first-line chemotherapy.

Methods

5-FU IC50 was determined in CRC cell lines DLD1, LoVo, and HCT-15 applying MTT assays. mRNA expression of FGF2 was measured by RT-qPCR with HPRT as reference gene. Threshold values were determined by minimum p-value method. FGF2 expression was knocked down by sh (short hairpin) RNA in vitro. FGF receptor (FGF-R) was inhibited using Dovitinib with DMSO as control. In vitro results were were translated on the randomized FIRE1 trial (5-FU/LV/irinotecan [FUFIRI] vs. irinotecan/oxaliplatin [mIrOx] using Nanostring technology. 187 patients were included in this analysis.

Results

48 h incubation of CRC cell lines with 5-FU showed an increase of FGF2 expression [DLD1: 1.98-fold, p 

Conclusions

FGF2 expression might reflect chemoresistance in CRC cell lines as a knockdown of FGF2 led to a decrease of IC50 for 5-FU in vitro. In FIRE1, high FGF2 expression was associated with lower response rate and overall survival significantly. Interfering the FGF2 system might be a modulator for acquired chemoresistance.

Clinical trial identification

Legal entity responsible for the study

Department of Medicine III, University of Munich; Institute of Pathology, University of Munich

Funding

Weigand-Bohnewand-Gravenhorst-Fond, University of Munich

Disclosure

All authors have declared no conflicts of interest.

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