Fibroblast growth factor 2 orchestrates angiogenic networking in non-GIST STS patients

Thomas K Kilvaer1, Andrej Valkov, Sveinung W Sorbye

  • 1Institute of Medical Biology, University of Tromso, PB 9037, Tromso, Norway. Kilvaer@gmail.com

Abstract

Insights

High expression of fibroblast growth factor 2 (FGF2), alone or with PDGF-B and VEGFR-3, indicates poor prognosis in non-gastrointestinal stromal tumor soft-tissue sarcoma (non-GIST STS) patients. This finding aids in predicting survival outcomes for these rare cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Non-gastrointestinal stromal tumor soft-tissue sarcomas (non-GIST STSs) are aggressive and heterogeneous cancers.
  • Fibroblast growth factor 2 (FGF2), FGFR-1, PDGF-B, and VEGFR-3 are implicated in tumor angiogenesis.
  • Understanding the prognostic markers in non-GIST STSs is crucial for patient outcomes.

Purpose of the Study:

  • To investigate the prognostic significance of FGF2 and FGFR-1 in non-GIST STSs.
  • To explore the combined prognostic impact of FGF2 with PDGF-B and VEGFR-3.
  • To identify reliable biomarkers for predicting disease-specific survival in non-GIST STS patients.

Main Methods:

  • Tumor samples from 108 non-GIST STS patients were analyzed.
  • Tissue microarrays were constructed for comprehensive analysis.
  • Immunohistochemistry was employed to assess the expression levels of FGF2, FGFR-1, PDGF-B, and VEGFR-3.

Main Results:

  • High FGF2 expression was a significant independent predictor of poor disease-specific survival (P = 0.024).
  • Co-expression of FGF2 with PDGF-B showed a strong association with poor prognosis (overall P = 0.007; high co-expression HR = 6.0).
  • Co-expression of FGF2 with VEGFR-3 also indicated poorer survival outcomes (high co-expression P = 0.028, HR = 2.6).

Conclusions:

  • FGF2 is a significant negative prognosticator in non-GIST STSs.
  • The co-expression patterns of FGF2 with PDGF-B and VEGFR-3 further refine prognostic predictions.
  • These findings highlight FGF2-related pathways as potential therapeutic targets in non-GIST STSs.

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