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    Expression of Fas (CD95/APO-1) ligand by human breast cancers: significance for tumor immune privilege.

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    Authors
    O'Connell, J
    Bennett, M W
    O'Sullivan, G C
    O'Callaghan, J
    Collins, J K
    Shanahan, F
    Affiliation
    Department of Medicine, Cork University Hospital, National University of Ireland,, Cork, Ireland.
    Issue Date
    2012-02-03T15:13:33Z
    MeSH
    Antigens, CD95/biosynthesis
    Breast Neoplasms/*chemistry/pathology
    Fas Ligand Protein
    Female
    Humans
    Immunoblotting
    Immunohistochemistry
    Lymphocytes/chemistry
    Lymphocytes, Tumor-Infiltrating/chemistry
    Membrane Glycoproteins/*genetics
    Neurons/chemistry
    RNA, Messenger/analysis
    Receptors, Tumor Necrosis Factor/biosynthesis
    Reverse Transcriptase Polymerase Chain Reaction
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    Citation
    Clin Diagn Lab Immunol. 1999 Jul;6(4):457-63.
    Journal
    Clinical and diagnostic laboratory immunology
    URI
    http://hdl.handle.net/10147/209149
    PubMed ID
    10391843
    Abstract
    Breast cancers have been shown to elicit tumor-specific immune responses. As in other types of cancer, the antitumor immune response fails to contain breast tumor growth, and a reduction in both the quantity and cytotoxic effectiveness of tumor-infiltrating lymphocytes (TILs) is associated with a poorer prognosis. Fas ligand (FasL) induces apoptotic death of activated lymphocytes that express its cell surface receptor, FasR (CD95/APO-1). FasL-mediated apoptosis of activated lymphocytes contributes to normal immune downregulation through its roles in tolerance acquisition, immune response termination, and maintenance of immune privilege in the eye, testis, and fetus. In this report, we demonstrate that breast carcinomas express FasL. Using in situ hybridization and immunohistochemistry, we show that breast tumors constitutively express FasL at both the mRNA and protein levels, respectively. FasL expression is prevalent in breast cancer: 100% of breast tumors (17 of 17) were found to express FasL, and expression occurred over more than 50% of the tumor area in all cases. By immunohistochemistry, FasR was found to be coexpressed with FasL throughout large areas of all the breast tumors. This suggests that the tumor cells had acquired intracellular defects in FasL-mediated apoptotic signaling. FasL and FasR expression were independent of tumor type or infiltrative capacity. FasL expressed by tumor cells has previously been shown to kill Fas-sensitive lymphoid cells in vitro and has been associated with apoptosis of TILs in vivo. We conclude that mammary carcinomas express FasL in vivo as a potential inhibitor of the antitumor immune response.
    Language
    eng
    ISSN
    1071-412X (Print)
    1071-412X (Linking)
    Collections
    Cork University Hospital

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