期刊论文详细信息
Journal for ImmunoTherapy of Cancer
Oncogene withdrawal engages the immune system to induce sustained cancer regression
Dean W Felsher1  Alice C Fan1  Yulin Li1  Stephanie C Casey1 
[1] Division of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, 269 Campus Drive, CCSR 1105, Stanford 94305-5151, CA, USA
关键词: Tumor immunology;    Tumor microenvironment;    MYC;    Oncogene addiction;   
Others  :  1139877
DOI  :  10.1186/2051-1426-2-24
 received in 2014-03-11, accepted in 2014-06-06,  发布年份 2014
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【 摘 要 】

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.

【 授权许可】

   
2014 Casey et al.; licensee BioMed Central Ltd.

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