期刊
JOURNAL FOR IMMUNOTHERAPY OF CANCER
卷 2, 期 -, 页码 -出版社
BMJ PUBLISHING GROUP
DOI: 10.1186/2051-1426-2-24
关键词
Oncogene addiction; MYC; Tumor microenvironment; Tumor immunology
资金
- Burroughs Welcome Fund Career Award
- Damon Runyon Foundation Lilly Clinical Investigator Award
- NIH NCI [K23 CA140722]
- NIH R01 [CA 089305, 105102, 170378 PQ22, U54CA149145, U54CA143907]
- National Cancer Institute's In-vivo Cellular and Molecular Imaging Center [CA 114747]
- Integrative Cancer Biology Program [CA 112973]
- NIH/NCI PO1 [CA034233]
- Leukemia and Lymphoma Society Translational Research [R6223-07]
- NIH [5 T32 AI07290]
- NIH NRSA from the NCI [F32CA177139]
The targeted inactivation of a single oncogene can induce dramatic tumor regression, suggesting that cancers are oncogene addicted. Tumor regression following oncogene inactivation has been thought to be a consequence of restoration of normal physiological programs that induce proliferative arrest, apoptosis, differentiation, and cellular senescence. However, recent observations illustrate that oncogene addiction is highly dependent upon the host immune cells. In particular, CD4+ helper T cells were shown to be essential to the mechanism by which MYC or BCR-ABL inactivation elicits oncogene withdrawal. Hence, immune mediators contribute in multiple ways to the pathogenesis, prevention, and treatment of cancer, including mechanisms of tumor initiation, progression, and surveillance, but also oncogene inactivation-mediated tumor regression. Data from both the bench and the bedside illustrates that the inactivation of a driver oncogene can induce activation of the immune system that appears to be essential for sustained tumor regression.
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