4.7 Review

The MYC oncogene is a global regulator of the immune response

Journal

BLOOD
Volume 131, Issue 18, Pages 2007-2015

Publisher

AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2017-11-742577

Keywords

-

Categories

Funding

  1. National Institutes of Health (NIH), National Cancer Institute (NCI) [U01CA188383, R01CA208735]
  2. SPARK
  3. NCI [1F32CA177139]
  4. NIH Stanford University Cellular and Molecular Immunobiology Training Grant from the National Institute of Allergy and Infectious Diseases [5 T32AI07290]
  5. NATIONAL CANCER INSTITUTE [F32CA177139, R01CA208735, U01CA188383] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007290] Funding Source: NIH RePORTER

Ask authors/readers for more resources

The MYC proto-oncogene is a gene product that coordinates the transcriptional regulation of a multitude of genes that are essential to cellular programs required for normal as well as neoplastic cellular growth and proliferation, including cell cycle, self-renewal, survival, cell growth, metabolism, protein and ribosomal biogenesis, and differentiation. Here, we propose that MYC regulates these programs in a manner that is coordinated with a global influence on the host immune response. MYChad been presumed to contribute to tumorigenesis through tumor cell-intrinsic influences. More recently, MYC expression in tumor cells has been shown to regulate the tumor microenvironment through effects on both innate and adaptive immune effector cells and immune regulatory cytokines. Then, MYC was shown to regulate the expression of the immune checkpoint gene products CD47 and programmed death-ligand 1. Similarly, other oncogenes, which are known to modulate MYC, have been shown to regulate immune checkpoints. Hence, MYC may generally prevent highly proliferative cells from eliciting an immune response. MYC-driven neoplastic cells have coopted this mechanism to bypass immune detection. Thus, MYC inactivation can restore the immune response against a tumor. MYC-induced tumors may be particularly sensitive to immuno-oncology therapeutic interventions.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available