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Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma

Nils C Lehnen1, Anne von Mässenhausen, Holger Kalthoff

  • 1Institute of Pathology, University Hospital of Bonn, Bonn, Germany.

Histopathology
|July 2, 2013
PubMed
Abstract

Insights

Fibroblast growth factor receptor 1 (FGFR1) amplification occurs in a small subset of pancreatic cancers. Targeting FGFR1 with inhibitors like BGJ398 shows promise for treating these specific pancreatic ductal adenocarcinoma (PDAC) tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Pancreatic ductal adenocarcinomas (PDACs) exhibit chemoresistance, leading to poor patient survival.
  • Novel molecular targets are crucial for treating PDAC, especially in genetically defined subsets.
  • Tyrosine kinase receptor inhibitors (TKIs) are an established class of therapeutic agents.

Purpose of the Study:

  • To investigate the gene copy number and expression of fibroblast growth factor receptor 1 (FGFR1) in 155 PDAC patients.
  • To evaluate the efficacy of the FGFR-specific inhibitor BGJ398 against FGFR1-amplified pancreatic cancer cells in vitro.

Main Methods:

  • Fluorescence in-situ hybridization (FISH) and immunohistochemistry on 155 PDAC tissue microarrays.
  • Sequence analysis to identify genetic mutations.
  • In vitro proliferation assays using the PT45P1 cell line treated with BGJ398.

Main Results:

  • FGFR1 amplification was detected in 2.6% (4/155) of PDAC cases.
  • FGFR1 expression was observed in 4% (5/125) of tumors.
  • All FGFR1-amplified cases harbored an activating KRAS mutation (exon 2).
  • The FGFR1-amplified cell line PT45P1 demonstrated high FGFR1 mRNA and protein levels and its proliferation was inhibited by BGJ398.

Conclusions:

  • FGFR1 is a potential therapeutic target in a subset of PDAC patients with FGFR1-amplified tumors.
  • Identifying FGFR1 amplification may aid in preselecting patients for TKI-based therapies.
  • This finding could be important for interpreting clinical studies involving TKIs in PDAC.
Keywords:
amplificationfibroblast growth factor receptor 1fluorescence in-situ hybridizationpancreatic ductal adenocarcinoma

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