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TEM8/ANTXR1 blockade inhibits pathological angiogenesis and potentiates tumoricidal responses against multiple cancer

Amit Chaudhary1, Mary Beth Hilton, Steven Seaman

  • 1Tumor Angiogenesis Section, Mouse Cancer Genetics Program, National Cancer Institute (NCI), National Institutes of Health (NIH), Frederick, MD 21702, USA.

Cancer Cell
|February 21, 2012
PubMed

Insights

Targeting Tumor Endothelial Marker 8 (TEM8) shows promise for cancer therapy. Antibodies against TEM8 inhibit tumor growth and angiogenesis, offering a selective approach with potential to enhance existing treatments without added toxicity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Current antiangiogenic therapies for cancer exhibit limited efficacy and cause normal tissue toxicities.
  • There is a critical need for more selective therapeutic agents targeting pathological angiogenesis in tumors.

Purpose of the Study:

  • To investigate the role of Tumor Endothelial Marker 8 (TEM8), also known as Anthrax Toxin Receptor 1 (ANTXR1), in tumor growth and angiogenesis.
  • To evaluate the therapeutic potential of targeting TEM8 using antibodies.

Main Methods:

  • Genetic disruption of Tem8 in mouse models.
  • Development and testing of antibodies against the TEM8 extracellular domain.
  • Assessment of tumor xenograft growth, angiogenesis inhibition, and combination therapy efficacy in various cancer types (melanoma, breast, colon, lung).

Main Results:

  • Genetic disruption of Tem8 impaired the growth of diverse human tumor xenografts.
  • Antibodies targeting TEM8 blocked anthrax intoxication, inhibited tumor-induced angiogenesis, and demonstrated broad antitumor activity.
  • TEM8-targeted antibodies augmented the efficacy of existing anticancer agents without increasing toxicity.

Conclusions:

  • TEM8 is a viable target for selective inhibition of pathological angiogenesis.
  • Targeting TEM8 represents a promising strategy for novel cancer therapeutics with potential for combination therapy.

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