Haoqiang Ying

Abstract Adenosine deaminase acting on RNA 1 (ADAR1) contributes to immunotherapy resistance by suppressing interferon signaling. Therapeutic targeting of ADAR1 has not been achieved to date in clinical settings. Here, we discover all-trans retinoic acid (ATRA) promotes ADAR1 protein degradation in cancer. In addition, ATRA induces PD-L1 and combination of ATRA and PD-1 blockade reprograms tumor microenvironments to unleash antitumor immunity, thereby impeding tumor growth.

Correction to: Nature https://doi.org/10.1038/nature13611 Published online 10 August 2014 Since the version of the article initially published, a sample mislabeling issue has been brought to the authors’ attention concerning the immunoblots shown in Figs. 4a and 2b. The samples in Fig. 4a should have been labeled as “No. 3” and “No. 4”, rather than “No. 1” and “No. 2” as originally indicated. An updated version of Fig. 4a with the corrected sample identifiers is shown below as Fig. 1.

ArticleVolume 7, Issue 2102613Open access Affiliations & Notes 1Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 2The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, TX, USA 3Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA 4Department of Genomic Medicine, The University of Texas MD Anderson Cancer...