Chimeric Antigen Receptor T Cells in Acute Myeloid Leukemia

Katherine Cummins; Saar Gill

doi:10.1016/j.hoc.2023.06.004

Chimeric Antigen Receptor T Cells in Acute Myeloid Leukemia

Hematol Oncol Clin North Am. 2023 Dec;37(6):1125-1147. doi: 10.1016/j.hoc.2023.06.004. Epub 2023 Jul 11.

Authors

Katherine Cummins¹, Saar Gill²

Affiliations

¹ Peter MacCallum Cancer Centre, University of Melbourne, 305 Grattan Street, Melbourne, VIC 3000, Australia.
² Division of Hematology-Oncology, University of Pennsylvania Perelman School of Medicine, 8-101 Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA. Electronic address: saar.gill@pennmedicine.upenn.edu.

PMID: 37442676
DOI: 10.1016/j.hoc.2023.06.004

Abstract

Up to 30% of patients with acute myeloid leukemia (AML) who undergo chimeric antigen receptor (CAR) T-cell therapy have evidence of response, although trials are highly heterogeneous. These responses are rarely deep or durable. CD123, CD33, and CLL-1 have emerged as the most common targets for CAR T cells in AML. CAR T cells against myeloid antigens cause myeloablation as well as cytokine release syndrome, although neurotoxicity is rarely seen. Future efforts should focus on AML-specific antigen discovery or engineering, and on further enhancing the activity of CAR T cells.

Keywords: Acute myeloid leukemia; CAR T cells; CRS; Cellular immunotherapy; Myeloablation.

Publication types

Review