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Open Access Review

Oncogene withdrawal engages the immune system to induce sustained cancer regression

Stephanie C Casey, Yulin Li, Alice C Fan and Dean W Felsher*

Author Affiliations

Division of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, 269 Campus Drive, CCSR 1105, Stanford 94305-5151, CA, USA

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Journal for ImmunoTherapy of Cancer 2014, 2:24  doi:10.1186/2051-1426-2-24

Published: 15 July 2014

Abstract

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.

Keywords:
Oncogene addiction; MYC; Tumor microenvironment; Tumor immunology