Oncogenic drivers dictate immune control of acute myeloid leukemia.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 37059710.
- Also identified by DOI 10.1038/s41467-023-37592-9 and PMC identifier 10104832.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Acute myeloid leukemia (AML) is a genetically heterogeneous, aggressive hematological malignancy induced by distinct oncogenic driver mutations. The effect of specific AML oncogenes on immune activation or suppression is unclear. Here, we examine immune responses in genetically distinct models of AML and demonstrate that specific AML oncogenes dictate immunogenicity, the quality of immune response and immune escape through immunoediting. Specifically, expression of Nras<sup>G12D</sup> alone is sufficient to drive a potent anti-leukemia response through increased MHC Class II expression that can be overcome with increased expression of Myc. These data have important implications for the design and implementation of personalized immunotherapies for patients with AML.
Medical subject headings
- Leukemia, Myeloid, Acute
- Hematologic Neoplasms