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Updated: May 29, 2026

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth
06:35

A Mouse Model to Investigate the Role of Cancer-Associated Fibroblasts in Tumor Growth

Published on: December 22, 2020

Fibroblast growth factor signaling in non-small-cell lung cancer

Thomas J Semrad1, Philip C Mack

  • 1Division of Hematology/Oncology, Department of Internal Medicine, University of California, Davis, Sacramento, CA 95817, USA. thomas.semrad@ucdmc.ucdavis.edu

Clinical Lung Cancer
|October 1, 2011
PubMed

Insights

Fibroblast growth factor (FGF) signaling drives non-small cell lung cancer (NSCLC) growth and resistance to targeted therapies. Targeting the FGF pathway offers a promising strategy for improving NSCLC treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Non-small cell lung cancer (NSCLC) treatment outcomes remain suboptimal despite advances targeting EGFR and VEGF pathways.
  • Emerging evidence implicates fibroblast growth factor (FGF) signaling in NSCLC pathogenesis, progression, and resistance to existing therapies.

Purpose of the Study:

  • To review the structure and function of the FGF signaling pathway in NSCLC.
  • To evaluate the role of FGF signaling in angiogenesis and proliferation in NSCLC.
  • To discuss FGF pathway inhibitors as a therapeutic strategy for NSCLC.

Main Methods:

  • Literature review of studies on FGF signaling in NSCLC.
  • Analysis of FGF ligand and receptor expression as prognostic biomarkers.
  • Evaluation of clinical development of FGF receptor (FGFR) inhibitors.

Main Results:

  • FGF signaling contributes to NSCLC pathogenesis through autocrine loops, promoting angiogenesis and proliferation.
  • FGF pathway activation may mediate resistance to anti-EGFR and anti-VEGF therapies.
  • FGF ligand and receptor expression show potential as prognostic biomarkers in NSCLC.

Conclusions:

  • The FGF signaling pathway is a critical driver in NSCLC and a potential mechanism of therapeutic resistance.
  • Targeting FGFR with specific inhibitors is a promising therapeutic avenue for NSCLC treatment.
  • Further research into FGF pathway modulation is warranted for improved lung cancer therapies.

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