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      CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation.

      Cancer Cell
      Animals, Apoptosis, physiology, CD4-Positive T-Lymphocytes, immunology, Cell Aging, drug effects, Cell Proliferation, Chemokines, genetics, metabolism, Cyclosporine, pharmacology, Fusion Proteins, bcr-abl, Gene Expression Regulation, Neoplastic, Gene Silencing, Immunosuppressive Agents, Leukemia, Experimental, Mice, Mice, Transgenic, Neoplasms, pathology, Neovascularization, Pathologic, Oncogenes, Proto-Oncogene Proteins c-myc, Remission Induction, Thrombospondin 1, Tumor Microenvironment

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          Abstract

          Oncogene addiction is thought to occur cell autonomously. Immune effectors are implicated in the initiation and restraint of tumorigenesis, but their role in oncogene inactivation-mediated tumor regression is unclear. Here, we show that an intact immune system, specifically CD4(+) T cells, is required for the induction of cellular senescence, shutdown of angiogenesis, and chemokine expression resulting in sustained tumor regression upon inactivation of the MYC or BCR-ABL oncogenes in mouse models of T cell acute lymphoblastic lymphoma and pro-B cell leukemia, respectively. Moreover, immune effectors knocked out for thrombospondins failed to induce sustained tumor regression. Hence, CD4(+) T cells are required for the remodeling of the tumor microenvironment through the expression of chemokines, such as thrombospondins, in order to elicit oncogene addiction. Copyright © 2010 Elsevier Inc. All rights reserved.

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