Abstract
Leukemia-initiating cells of core binding factor (CBF) acute myeloid leukemia (AML) likely derive from early committed hematopoietic precursors expressing CD33. As such, targeting CD33 could ameliorate the chance of cure of CBF AML patients. We compared 12 CBF AML patients treated with Fludarabine, Cytarabine, Idarubicin and Gemtuzumab Ozogamicin (FLAI-GO regimen) with 25 CBF AML patients treated with the same schedule, but without GO. With the limit of small numbers, we observed a consistent trend toward better overall survival, disease free survival and event free survival in the FLAI-GO group. We also demonstrated the ability of GO to induce the disappearance in vitro of the AML1-ETO molecular transcript in a polymerase chain reaction-positive graft without decreasing the clonogenic potential of CD34+/CD38- cells. This represent the proof of principle for using GO in a purging strategy before autologous stem cell transplantation. Therefore, our data argue in favor of the reinstitution of GO in the therapy of CBF AML.
Highlights
40-50%.1 As such, efforts have been made to increase the dose intensity of first line treatment over the standard
In order to address the role of GO in the treatment of core binding factor (CBF) acute myeloid leukemia (AML), we retrospectively reviewed 12 CBF AML patients [t(8;21)
The potential of GO in the treatment of CBF AML is based on strong biological bases: first of all, most t(8;21) AML blasts do not express the transporter P-glycoprotein (Pgp),12 i.e. the Multi-Drug Resistance 1 (MDR1) gene product, and this seems related to a selective repression of the promoter of MDR1 by AML1-ETO.13
Summary
40-50%.1 As such, efforts have been made to increase the dose intensity of first line treatment over the standard.
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