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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

Updated: May 20, 2025

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
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Vascular Endothelial Growth Factor Receptors in the Vascularization of Pancreatic Tumors: Implications for Prognosis

Craig Grobbelaar1, Vanessa Steenkamp2, Peace Mabeta1

  • 1Department of Physiology, School of Medicine, Faculty of Health Sciences, University of Pretoria, Pretoria 0002, South Africa.

Current Issues in Molecular Biology
|March 26, 2025
PubMed
Summary

Vascular endothelial growth factor (VEGF) and its receptor (VEGFR)-2 drive pancreatic cancer but therapies face resistance. This review examines VEGFR roles and strategies like combination treatments to improve outcomes.

Keywords:
VEBFR-3VEGFR-1VEGFR-2angiogenesishypoxialymphangiogenesismetastasispancreatic cancertumor microenvironmentvascular homeostasis

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Area of Science:

  • Oncology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Vascular endothelial growth factor (VEGF) and its receptor (VEGFR)-2 are key drivers of angiogenesis and metastasis in pancreatic cancer (PC).
  • Overexpression of VEGF and VEGFR-2 correlates with poor prognosis and advanced disease stages in PC patients.
  • Current therapies targeting VEGF/VEGFR-2 show limited efficacy due to resistance mechanisms, often involving alternative vascularization pathways.

Purpose of the Study:

  • To explore the diverse roles of VEGFRs, including VEGFR-1 and VEGFR-3, in pancreatic cancer progression.
  • To review the mechanisms of resistance encountered with current anti-VEGF/VEGFR-2 therapies.
  • To discuss potential strategies for enhancing the efficacy of VEGFR-targeting treatments in PC.

Main Methods:

  • Literature review of studies on VEGF, VEGFRs, and their roles in pancreatic cancer.
  • Analysis of resistance mechanisms to anti-angiogenic therapies.
  • Exploration of novel therapeutic strategies and biomarkers.

Main Results:

  • VEGF and VEGFR-2 are critical for PC angiogenesis and metastasis, impacting patient survival.
  • Resistance to targeted therapies often involves activation of alternative signaling pathways.
  • VEGFR-1 and VEGFR-3 also play roles in PC, suggesting broader therapeutic targeting opportunities.

Conclusions:

  • Targeting VEGF/VEGFR-2 pathways in pancreatic cancer is crucial but complicated by resistance.
  • Combination therapies, development of selective inhibitors, and biomarker utilization are promising avenues to overcome resistance.
  • A comprehensive understanding of all VEGFR family members' roles is essential for improving PC treatment outcomes.