Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours

B. M. Fenton*, S. F. Paoni, W. Liu, S. Y. Cheng, B. Hu, I. Ding

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


Vascular endothelial growth factor (VEGF) is an intensively studied molecule that has significant potential, both in stimulating angiogenesis and as a target for antiangiogenic approaches. We utilised MCF-7 breast cancer cells transfected with either of two of the major VEGF isoforms, VEGF 121 or VEGF165, or fibroblast growth factor-1 (FGF-1) to distinguish the effects of these factors on tumour growth, vascular function, and oxygen delivery. While each transfectant demonstrated substantially increased tumorigenicity and growth rate compared to vector controls, only VEGF121 produced a combination of significantly reduced total and perfused vessel spacing, as well as a corresponding reduction in overall tumour hypoxia. Such pathophysiological effects are of potential importance, since antiangiogenic agents designed to block VEGF isoforms could in turn result in the development of therapeutically unfavourable environments. If antiangiogenic agents are also combined with conventional therapies such as irradiation or chemotherapy, microregional deficiencies in oxygenation could play a key role in ultimate therapeutic success.

Original languageEnglish (US)
Pages (from-to)430-435
Number of pages6
JournalBritish Journal of Cancer
Issue number2
StatePublished - Jan 26 2004


  • Antiangiogenic
  • Hypoxia
  • Image analysis
  • Perfusion
  • Tumour vasculature

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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