Acute Myeloid Leukemia with FLT3 internal tandem duplication mutations (FLT3-ITDmut AML) is an aggressive leukemia character- ized by heterogeneous genetic landscape [1]. Despite significant advances in AML therapy, the relapse rate remains high, due to the emergence of resistant clones, possibly involving leukemic stem cells (LSCs) [2]. This highlights the unmet need for deeper understanding of the molecular and immunophenotypic land- scape of LSCs in FLT3-ITDmut AML. We previously identified a population of leukemic precursor cells (LPCs), present at the time of initial AML diagnosis, characterized by the CD34/CD123/CD25/ CD99+ immunophenotype, and predictive for FLT3-ITDmut positivity [3]. In particular, these cells overexpress CD99 antigen, which may represent a target for monoclonal antibody (mAb) treatment [4]
Travaglini, S., Ottone, T., Angelini, D. F., Fiori, V., Dominici, S., Noguera, N. I., Sniegocka, M., Antonelli, S., Irno Consalvo, M. A., De Bardi, M., Banella, C., Divona, M., Marchesi, F., Masciarelli, S., Fazi, F., Pieraccioli, M., Palmieri, R., De Angelis, G., Buccisano, F., Venditti, A., Battistini, L., Magnani, M., Voso, M. T., CD99 as a novel therapeutic target on leukemic progenitor cells in FLT3-ITDmut AML, <<LEUKEMIA>>, 2022; 36 (6): 1685-1688. [doi:10.1038/s41375-022-01566-5] [http://hdl.handle.net/10807/217699]
CD99 as a novel therapeutic target on leukemic progenitor cells in FLT3-ITDmut AML
Masciarelli, SilviaMembro del Collaboration Group
;
2022
Abstract
Acute Myeloid Leukemia with FLT3 internal tandem duplication mutations (FLT3-ITDmut AML) is an aggressive leukemia character- ized by heterogeneous genetic landscape [1]. Despite significant advances in AML therapy, the relapse rate remains high, due to the emergence of resistant clones, possibly involving leukemic stem cells (LSCs) [2]. This highlights the unmet need for deeper understanding of the molecular and immunophenotypic land- scape of LSCs in FLT3-ITDmut AML. We previously identified a population of leukemic precursor cells (LPCs), present at the time of initial AML diagnosis, characterized by the CD34/CD123/CD25/ CD99+ immunophenotype, and predictive for FLT3-ITDmut positivity [3]. In particular, these cells overexpress CD99 antigen, which may represent a target for monoclonal antibody (mAb) treatment [4]
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