AML1-ETO inhibits acute myeloid leukemia immune escape by CD48. Issue 4 (21st March 2021)

• Record Type: Journal Article
• Authors: Wang, Zhiding; Guan, Wei; Wang, Mengzhen; Chen, Jinghong; Zhang, Linlin; Xiao, Yang; Wang, Lixin; Li, Yonghui; Yu, Li
• Is Part Of: Leukemia & lymphoma. Volume 62:Issue 4(2021)
• Page Start: 937
• Page End: 943
• Publication Date: 2021-03-21
• Subjects: AML1-ETO; -- AML; -- CD48; -- acetylation; -- NK; Leukemia -- Periodicals; Lymphomas -- Periodicals; 616.99419
• DOI: 10.1080/10428194.2020.1849680
• Languages: English
• ISSNs: 1042-8194

Abstract

Abstract: The t(8;21)(q22;q22) translocation is the most common chromosomal translocation in acute myeloid leukemia (AML), and it gives rise to acute myeloid gene 1 (AML1)-myeloid transforming gene 8 (ETO)-positive AML, which has a relatively favorable prognosis. CD48 is a favorable prognosis factor that is downregulated in AML patients. AML can escape immunosurveillance of natural killer (NK) cells by decreasing CD48 expression. The correlation between AML1-ETO and CD48-mediated immune evasion is not well understood. Here, we show that AML1-ETO can increase CD48 expression, which is regulated by AML1-ETO/P300-mediated acetylation. AML1-ETO can inhibit AML immune escape from NK cell recognition and killing by increasing CD48 expression. This study describes a novel mechanism by which AML1-ETO can inhibit AML immune escape by increasing CD48 acetylation, thereby providing new evidence about AML patients with AML1-ETO oncogene infusion having better clinical outcomes.