Imaging the modulation of adenoviral kinetics and biodistribution for cancer gene therapy

Mol Ther. 2007 May;15(5):921-9. doi: 10.1038/mt.sj.6300119. Epub 2007 Mar 13.

Abstract

To explore systemic utilization of Epstein-Barr virus (EBV)-specific transcriptionally targeted adenoviruses, three vectors were constructed to examine kinetics, specificity, and biodistribution: adv.oriP.luc, expressing luciferase under EBV-specific control; adv.SV40luc, expressing luciferase constitutively; and adv.oriP.E1A.oriP.luc, a conditionally replicating adenovirus, expressing both luciferase and E1A. Bioluminescence imaging (BLI) was conducted on tumor-bearing severe combined immunodeficient (SCID) mice (C666-1, EBV-positive human nasopharyngeal cancer) treated intravenously (i.v.) with 3 x 10(8) infectious units (ifu) of the adenoviral vectors. At 72 hours, adv.oriPluc demonstrated an 8.4-fold higher tumor signal than adv.SV40luc; adv.oriP.E1A.oriP.luc was 26.7-fold higher; however, a significant liver signal was also observed, necessitating further action to improve biodistribution. Several compounds were examined to this end, including norepinephrine, serotonin, clodronate liposomes, and STI571, to determine whether any of these measures could improve adenoviral biodistribution. Each of these interventions was assessed using BLI in mice i.v. injected with adv.oriP.luc. STI571 achieved the highest increase in tumor-to-liver ratio (TLR; 6.6-fold), which was associated with a 59% reduction in tumor interstitial fluid pressure (IFP) along with a decrease in platelet-derived growth factor-beta receptor (PDGF beta R) activation. This study reports the favorable modulation by STI571 of the biodistribution of adenoviral vectors, providing a potential approach to improving therapeutic outcome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics
  • Animals
  • Antineoplastic Agents / pharmacology
  • Benzamides
  • Cell Line, Tumor
  • Clodronic Acid / pharmacology
  • Genetic Therapy / methods*
  • Genetic Vectors / genetics
  • Humans
  • Imatinib Mesylate
  • Immunohistochemistry
  • Kinetics
  • Liver / metabolism
  • Luciferases / genetics
  • Luciferases / metabolism
  • Luminescent Measurements / methods
  • Male
  • Mice
  • Mice, SCID
  • Microscopy, Fluorescence
  • Neoplasms / metabolism
  • Neoplasms / therapy*
  • Phosphorylation / drug effects
  • Piperazines / pharmacology
  • Pyrimidines / pharmacology
  • Receptor, Platelet-Derived Growth Factor beta / metabolism
  • Recombinant Fusion Proteins / administration & dosage
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / pharmacokinetics*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • Tissue Distribution / drug effects

Substances

  • Antineoplastic Agents
  • Benzamides
  • Piperazines
  • Pyrimidines
  • Recombinant Fusion Proteins
  • Clodronic Acid
  • Imatinib Mesylate
  • Luciferases
  • Receptor, Platelet-Derived Growth Factor beta