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Generation of an Orthotopic Xenograft of Pancreatic Cancer Cells by Ultrasound-Guided Injection
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Imaging and modulating antisense microdistribution in solid human xenograft tumor models.

Joseph D Mocanu1, Kenneth W Yip, Julia Skliarenko

  • 1Division of Applied Molecular Oncology, Ontario Cancer Institute, Canada.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|October 3, 2007
PubMed
Summary

Antisense oligodeoxynucleotides (ASO) accumulate in hypoxic and necrotic tumor regions. Novel algorithms quantify ASO distribution, showing reduced accumulation in vasculature after antivascular therapy, aiding combination therapy assessment.

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Area of Science:

  • Oncology
  • Pharmacology
  • Biomedical Engineering

Background:

  • The tumor microenvironment (TME) presents significant challenges for cancer therapeutics due to its heterogeneity, including irregular vasculature, hypoxia, and necrosis.
  • Understanding the biodistribution of therapeutic agents within the TME is crucial for optimizing treatment efficacy.
  • Antisense oligodeoxynucleotides (ASO) are a promising class of therapeutics, but their distribution in solid tumors remains poorly characterized.

Purpose of the Study:

  • To investigate the distribution patterns of systemically administered antisense oligodeoxynucleotides (ASO) within solid tumors.
  • To evaluate the utility of novel quantitative algorithms for assessing ASO biodistribution in relation to tumor microenvironment characteristics.
  • To examine the impact of antivascular therapy on ASO distribution within the TME.

Main Methods:

  • Fluorescein-labeled ASO and Hoechst 33342 were administered intravenously to tumor-bearing mice.
  • Tiled fluorescence stereomicroscopy and novel quantification algorithms were employed to analyze ASO distribution in tumor sections.
  • Tumor sections from four human xenograft models were analyzed for hypoxia, apoptosis/necrosis, and vascularization.

Main Results:

  • ASO consistently accumulated in hypoxic, necrotic, and apoptotic regions across all four tumor models.
  • A distinct pattern of ASO distribution relative to active vasculature was observed in each tumor model.
  • Pretreatment with the antivascular agent ZD6126 significantly reduced ASO accumulation in the vasculature of C666-1 xenografts, correlating with increased necrosis and reduced interstitial fluid pressure.

Conclusions:

  • The developed algorithms provide a generalizable and objective method for characterizing molecular therapeutic agent distribution within the TME.
  • Quantitative assessment of ASO distribution can be effectively achieved using these algorithms.
  • These methods can be utilized to evaluate the effects of combination therapies, such as antivascular agents, on drug delivery within tumors.