An essential role for the immune system in the mechanism of tumor regression following targeted oncogene inactivation

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

Research output: Contribution to journalReview articlepeer-review

10 Scopus citations

Abstract

Tumors are genetically complex and can have a multitude of mutations. Consequently, it is surprising that the suppression of a single oncogene can result in rapid and sustained tumor regression, illustrating the concept that cancers are often "oncogene addicted." The mechanism of oncogene addiction has been presumed to be largely cell autonomous as a consequence of the restoration of normal physiological programs that induce proliferative arrest, apoptosis, differentiation, and/or cellular senescence. Interestingly, it has recently become apparent that upon oncogene inactivation, the immune response is critical in mediating the phenotypic consequences of oncogene addiction. In particular, CD4+ T cells have been suggested to be essential to the remodeling of the tumor microenvironment, including the shutdown of host angiogenesis and the induction of cellular senescence in the tumor. However, adaptive and innate immune cells are likely involved. Thus, the effectors of the immune system are involved not only in tumor initiation, tumor progression, and immunosurveillance, but also in the mechanism of tumor regression upon targeted oncogene inactivation. Hence, oncogene inactivation may be an effective therapeutic approach because it both reverses the neoplastic state within a cancer cell and reactivates the host immune response that remodels the tumor microenvironment.

Original languageEnglish (US)
Pages (from-to)282-291
Number of pages10
JournalImmunologic Research
Volume58
Issue number2-3
DOIs
StatePublished - May 2014

Keywords

  • MYC
  • Oncogene addiction
  • Tumor immunology
  • Tumor microenvironment
  • Tumor recurrence

ASJC Scopus subject areas

  • Immunology

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