Letter
作者: Sumiyoshi, Teiko ; Daver, Naval ; Salhotra, Amandeep ; Jurcic, Joseph G. ; Cooper, James ; Li, Mengsong ; Brandwein, Joseph M. ; Assouline, Sarit ; Ma, Connie ; Vaze, Anjali ; Pollyea, Daniel A. ; Podoltsev, Nikolai A. ; Dere, Randall C. ; Pourmohamad, Tony ; Yee, Karen ; Samineni, Divya
Acute myeloid leukemia (AML) is an aggressive malignancy with especially dismal outcomes in relapsed or refractory patients. C-type lectin-like mol.-1 (CLL1) is a transmembrane glycoprotein expressed on the surface of AML blast cells.CLL1 is expressed on committed myeloid cells in bone marrow, but is absent on normal HSCs.Its expression is detectable on neutrophils and monocytes/macrophages but there is no known expression on non-hematopoietic stem cells (HSC) or tissues.The absence of CLL1 expression on HSC may translate into less myelosuppression than other AML targets.Reduced myelosuppression may increase the therapeutic window while also enabling better combinability with standard AML therapies.CLL1 as a target in AML continues to remain viable and the data presented here helps to elucidate its role, guide future development and potential pitfalls that should be considered with future CLL1 directed therapies in myeloid malignancies.