(99)mTc-(CO)(3) His-annexin A5 micro-SPECT demonstrates increased cell death by irinotecan during the vascular normalization window caused by bevacizumab

J Nucl Med. 2011 Nov;52(11):1786-94. doi: 10.2967/jnumed.111.092650.

Abstract

Colorectal tumors are dependent on angiogenesis for growth, and vascular endothelial growth factor (VEGF) is a key mediator of tumor angiogenesis. Antiangiogenic drugs can induce a transient normalization of the tumor vasculature with improved delivery of coadministered chemotherapy. The efficacy of antihuman VEGF antibody (bevacizumab) with or without irinotecan was evaluated in a colorectal cancer xenograft using (99m)Tc-(CO)(3) His-annexin A5.

Methods: Colo205-bearing mice were treated with a single dose of bevacizumab (5 mg/kg) during 2, 4, or 6 d. Microvessel density, pericyte coverage (α-smooth-muscle actin immunostaining), collagen-covered tumor vessels (Masson trichrome staining), and tumor hypoxic fraction (pimonidazole staining) were determined at the 3 different time points after treatment with bevacizumab. To investigate the possible synergistic effects of combination therapy with bevacizumab and irinotecan, Colo205-bearing mice were treated with a single dose of bevacizumab 2, 4, or 6 d before administration of a single dose of irinotecan (100 mg/kg) or 0.9% NaCl. The apoptosis-detecting radiotracer (99m)Tc-(CO)(3) His-annexin A5 was injected (18.5 MBq) in mice 12, 24, and 48 h after the start of the irinotecan or NaCl treatment, and micro-SPECT was subsequently performed 3.5 h after injection of the radiotracer. Results were correlated to histologic analysis for apoptosis (caspase-3 activation).

Results: Four days after bevacizumab administration, microvessel density decreased significantly, and α-smooth-muscle actin and collagen-covered vessels, compared with control tumors, were increased, suggesting normalization of the tumor vasculature. Hypoxic fraction was slightly reduced 4 d after treatment with bevacizumab. SPECT analyses demonstrated a significant increase in tumoral (99m)Tc-(CO)(3) His-annexin A5 uptake 4 d after bevacizumab treatment and 24 h after irinotecan administration (232.78 ± 24.82 percentage injected dose/tumor weight [g]/body weight [kg], P < 0.05), compared with each monotherapy, indicating a synergistic effect of both therapies.

Conclusion: (99m)Tc-(CO)(3) His-annexin A5 micro-SPECT demonstrates increased antitumor activity of irinotecan during the transient vascular normalization period caused by bevacizumab. Our data outline the importance of timing of combined anti-VEGF treatment with chemotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / genetics
  • Angiopoietin-1 / genetics
  • Animals
  • Annexin A5*
  • Antibodies, Monoclonal, Humanized / pharmacology*
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects*
  • Bevacizumab
  • Camptothecin / analogs & derivatives*
  • Camptothecin / pharmacology
  • Caspase 3 / metabolism
  • Cell Hypoxia / drug effects
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic
  • Colorectal Neoplasms / blood supply*
  • Colorectal Neoplasms / diagnostic imaging
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology
  • Female
  • Irinotecan
  • Mice
  • Microvessels / drug effects
  • Microvessels / metabolism
  • Neovascularization, Pathologic / drug therapy*
  • Organotechnetium Compounds*
  • Platelet Endothelial Cell Adhesion Molecule-1 / genetics
  • Tomography, Emission-Computed, Single-Photon*
  • Transcription, Genetic / drug effects
  • Tumor Burden / drug effects
  • Vascular Endothelial Growth Factor A / genetics

Substances

  • (99)mTc-(CO)(3) His-annexin A5
  • Actins
  • Angiopoietin-1
  • Annexin A5
  • Antibodies, Monoclonal, Humanized
  • Antineoplastic Agents
  • Organotechnetium Compounds
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Vascular Endothelial Growth Factor A
  • Bevacizumab
  • Irinotecan
  • Caspase 3
  • Camptothecin