Oncogene withdrawal engages the immune system to induce sustained cancer regression

Stephanie C. Casey, Yulin Li, Alice C. Fan, Dean W. Felsher

Research output: Contribution to journalReview articlepeer-review

12 Scopus citations

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.

Original languageEnglish (US)
Article number24
JournalJournal for immunotherapy of cancer
Volume2
Issue number1
DOIs
StatePublished - Jul 15 2014

Keywords

  • MYC
  • Oncogene addiction
  • Tumor immunology
  • Tumor microenvironment

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Molecular Medicine
  • Oncology
  • Pharmacology
  • Cancer Research

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