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Tumor endothelial marker 1 (Tem1) functions in the growth and progression of abdominal tumors

  1. Author:
    Nanda, A.
    Karim, B.
    Peng, Z. S.
    Liu, G. S.
    Qiu, W. P.
    Gan, C.
    Vogelstein, B.
    St Croix, B.
    Kinzler, K. W.
    Huso, D. L.
  2. Author Address

    Johns Hopkins Med Inst, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Ludwig Ctr Canc Genet & Therapeut, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Dept Comparat Med, Baltimore, MD 21205 USA. Johns Hopkins Med Inst, Howard Hughes Med Inst, Baltimore, MD 21205 USA. NCI, Tumor Angiogenesis Sect, Mouse Canc Genet Program, NIH, Frederick, MD 21702 USA Vogelstein, B, Johns Hopkins Med Inst, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA
    1. Year: 2006
    2. Date: FEB 28
  1. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 103
    2. 9
    3. Pages: 3351-3356
  2. Type of Article: Article
  1. Abstract:

    Tumor endothelial marker 1 (Tem1; endosialin) is the prototypical member of a family of genes expressed in the stroma of tumors. To assess the functional role of Tem1, we disrupted the Tem1 gene in mice by targeted homologous recombination. Tem1(-/-) mice were healthy, their wound healing was normal, and tumors grew normally when implanted in s.c. sites. However, there was a striking reduction in tumor growth, invasiveness, and metastasis after transplantation of tumors to abdominal sites in mice without functional Tem1 genes. These data indicate that the stroma can control tumor aggressiveness and that this control varies with anatomic site. Therefore, they have significant implications for the mechanisms underlying tumor invasiveness and for models that evaluate this process

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External Sources

  1. WOS: 000235780700063

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