Melinda Ann Biernacki, Jessica Lok, Ralph Graeme Black, Kimberly A Foster, Carrie Cummings, Kyle B Woodward, Tim Monahan, Vivian G Oehler, Derek L Stirewalt, David Wu, Anthony Rongvaux, Hans Joachim Deeg, Marie Bleakley
BACKGROUND: Myelodysplastic syndromes (MDS) arise from somatic mutations acquired in hematopoietic stem and progenitor cells, causing cytopenias and predisposing to transformation into secondary acute myeloid leukemia (sAML). Recurrent mutations in spliceosome genes, including U2AF1 , are attractive therapeutic targets as they are prevalent in MDS and sAML, arise early in neoplastic cells, and are generally absent from normal cells, including normal hematopoietic cells. MDS and sAML are susceptible to T cell-mediated killing, and thus engineered T-cell immunotherapies hold promise for their treatment...
December 12, 2023: Journal for Immunotherapy of Cancer