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T-bet Regulates Metastasis Rate in a Murine Model of Primary Prostate Cancer

¹ Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts;
² Departments of Internal Medicine and Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri; and
³ Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts

The local progression of primary tumors is extrinsically controlled by type 1 immune responses, particularly via the cytokine IFN-, whose secretion is highly dependent on helper T cells. The T-box transcription factor T-bet (Tbx21) plays a critical role in the development of type 1 helper T cells and is essential for the production of IFN-. Here, the T-bet pathway in the autochthonous transgenic adenocarcinoma mouse prostate model is demonstrated to have only a modest effect on the characteristics of primary prostate cancers but rather exerts a significant suppressor function in the development of metastatic disease.

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