Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia

In this study, we demonstrate that aberrant expression of SLAMF6 on acute myeloid leukemia (AML) cells serves as a novel immune escape mechanism that can be inhibited by antibodies against the SLAMF6 dimerization site. This constitutes a novel mechanism of checkpoint inhibition, which paves the way for immunotherapy in AML and other SLAMF6-expressing cancers. This study utilizes single cell sequencing data from the AML cell line HNT-34 co-cultured with normal T cells, with and without antibody targeting SLAMF6, as well as single cell data of 38 primary AML samples.

Type: RNASeq
Archiver: Federated European Genome-Phenome Archive (FEGA Sweden)

1 Dataset 1 Publication

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Dataset ID	Description	Technology	Samples
EGAD50000001573	This dataset contains fastq-files from single cell 5' RNA sequencing of the AML cell line HNT34 and normal T cells following co-culture with and without an antibody blocking SLAMF6 (TNC-1). The libraries were prepared using 10X GEM-X Universal 5' Gene Expression v3 Reagent Kit. In total, the dataset contains sequenced gene expression libraries from four samples (HNT34 co-cultured with T cells from two different donors; for both donors there is one sample with and one sample without the blocking antibody).	Illumina NovaSeq 6000	4

Publications	Citations
Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia. Sandén C, Landberg N, Peña-Martínez P, Thorsson H, Daga S, Puente-Moncada N, Rodriguez-Zabala M, von Palffy S, Rissler M, Lazarevic V, Juliusson G, Ohlin M, Hyrenius-Wittsten A, Orsmark-Pietras C, Lilljebjörn H, Ågerstam H, Fioretos T. Nat Cancer 6: 2025 1821-1838	0