MYC regulates the antitumor immune response through CD47 and PD-L1

Author:

Casey Stephanie C.1,Tong Ling1,Li Yulin1,Do Rachel1,Walz Susanne2,Fitzgerald Kelly N.1,Gouw Arvin M.1,Baylot Virginie1,Gütgemann Ines13,Eilers Martin24,Felsher Dean W.1

Affiliation:

1. Division of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.

2. Comprehensive Cancer Center Mainfranken, Core Unit Bioinformatics, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.

3. Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.

4. Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany.

Abstract

Oncogene control of antitumor immunity Recent clinical success of cancer immunotherapy has intensified interest in how tumors normally evade the immune response. Whether and how oncogenes contribute to this process are not well understood. In a study of mice, Casey et al. found that the MYC oncogene, which is aberrantly activated in many human cancers, up-regulates the expression of genes encoding proteins that dampen the antitumor response. These include two proteins that are often overexpressed on tumor cells and that serve as immune checkpoints. One of them (PDL1) sends to the immune system a “don't find me” signal, and the other (CD47) sends a “don't eat me” signal. Thus, therapies aimed at suppressing MYC may help promote an immune response against tumors. Science , this issue p. 227

Funder

Cancer Research Institute Clinic and Laboratory Innovation Program

NIH

Alex’s Lemonade Stand Foundation

Deutsche Forschungsgemeinschaft (DFG)

Deutsche Krebshilfe

DFG

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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