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TEM8/ANTXR1 Blockade Inhibits Pathological Angiogenesis and Potentiates Tumoricidal Responses against Multiple Cancer Types

  1. Author:
    Chaudhary, A.
    Hilton, M. B.
    Seaman, S.
    Haines, D. C.
    Stevenson, S.
    Lemotte, P. K.
    Tschantz, W. R.
    Zhang, X. Y. M.
    Saha, S.
    Fleming, T.
    St Croix, B.

  2. Author Address

    [Chaudhary, Amit; Hilton, Mary Beth; Seaman, Steven; St. Croix, Brad] NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA. [Hilton, Mary Beth] NCI, Basic Res Program, SAIC, NIH, Frederick, MD 21702 USA. [Haines, Diana C.] NCI, Vet Pathol Sect, Pathol Histotechnol Lab, SAIC,NIH, Frederick, MD 21702 USA. [Stevenson, Susan; Lemotte, Peter K.; Tschantz, William R.; Zhang, Xiaoyan M.; Saha, Saurabh; Fleming, Tony] Novartis Inst BioMed Res, Cambridge, MA 02139 USA.;St Croix, B (reprint author), NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA;stcroix@ncifcrf.gov
    1. Year: 2012
    2. Date: Feb
  2. Journal: Cancer Cell
    1. 21
    2. 2
    3. Pages: 212-226
  4. Type of Article: Article
  5. ISSN: 1535-6108
  1. Abstract:

    Current antiangiogenic agents used to treat cancer only partially inhibit neovascularization and cause normal tissue toxicities, fueling the need to identify therapeutic agents that are more selective for pathological angiogenesis. Tumor endothelial marker 8 (TEM8), also known as anthrax toxin receptor 1 (ANTXR1), is a highly conserved cell-surface protein overexpressed on tumor-infiltrating vasculature. Here we show that genetic disruption of Tem8 results in impaired growth of human tumor xenografts of diverse origin including melanoma, breast, colon, and lung cancer. Furthermore, antibodies developed against the TEM8 extracellular domain blocked anthrax intoxication, inhibited tumor-induced angiogenesis, displayed broad antitumor activity, and augmented the activity of clinically approved anticancer agents without added toxicity. Thus, TEM8 targeting may allow selective inhibition of pathological angiogenesis.

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External Sources

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  2. DOI: 10.1016/j.ccr.2012.01.004
  3. View record in Web of Science®
  4. WOS: 000300476000012

Library Notes

  1. Fiscal Year: FY2011-2012
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