Journal
CANCER CELL
Volume 18, Issue 5, Pages 485-498Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2010.10.002
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Funding
- Burroughs Welcome Fund
- Damon Runyon Foundation
- NIH [CA 089305, 105102, CA 118374]
- National Cancer Institute's In-vivo Cellular and Molecular Imaging Center [CA 114747]
- Integrative Cancer Biology Program [CA 112973]
- NIH/NCI [CA034233]
- Leukaemia and Lymphoma Society [R6223-07]
- Lymphoma Research Foundation
- Howard Hughes Medical Institute
- Stanford Medical Scholars Research Fellowship
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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.
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