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Tumor vessel stabilization and remodeling by anti-angiogenic therapy with bevacizumab

Philip Weisshardt1, Tanja Trarbach, Jan Dürig

  • 1Institute of Anatomy, University Hospital Essen, University of Duisburg-Essen, Hufelandstrasse 55, 45147 Essen, Germany. philip.weisshardt@gmx.de

Histochemistry and Cell Biology
|December 24, 2011
PubMed

Insights

Bevacizumab-resistant tumors show larger, stabilized vessels. Developing combination therapies is crucial to overcome resistance and improve anti-angiogenic treatment efficacy.

Area of Science:

  • Oncology
  • Vascular Biology
  • Pharmacology

Background:

  • Anti-angiogenic therapy, using agents like bevacizumab (anti-VEGF), targets tumor vascularization.
  • Tumor resistance to anti-angiogenic drugs is a significant clinical challenge.
  • Understanding mechanisms of resistance is vital for improving cancer treatment.

Purpose of the Study:

  • To characterize the vascular changes in bevacizumab-resistant human liver metastases.
  • To investigate the role of vascular remodeling and stabilization in anti-VEGF therapy resistance.
  • To explore potential strategies for overcoming treatment resistance.

Main Methods:

  • Analysis of human liver metastases from colorectal adenocarcinoma patients treated with bevacizumab.
  • Xenograft transplantation of human PC-3 prostate carcinoma cells in NOD SCID mice.
  • Combination therapy using bevacizumab and assessment of tumor vascularization and necrosis.

Main Results:

  • Bevacizumab-resistant tumor vessels exhibit increased diameter and normalized structures due to pericyte and smooth muscle cell recruitment.
  • Vascular stabilization occurs during anti-angiogenic therapy, leading to enhanced tumor necrosis.
  • Stabilized vessels show reduced susceptibility to bevacizumab, contributing to therapeutic resistance.

Conclusions:

  • Anti-angiogenic therapy induces vascular remodeling and stabilization, which paradoxically promotes resistance.
  • Developing second-generation combination therapies is essential to destabilize stabilized vessels.
  • Targeting vascular stabilization and subsequent destabilization may enhance anti-angiogenic treatment efficacy.

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