806 Priming for killing: Can the association GM-CSF-cytarabine have any role in the treatment of chronic myelogenous leukemia (CML)?

Except for bone marrow (BM) transplant, current therapies fail to cure CML because Ph’c1one cannot be eradicated. In vitro , exposing blastcrisis CML blasts to CM-CSF results in a three fold increment of cells in S phase and cell killing is 34% higher when GM-CSF+cytabarine are added simultaneously. This in vitro experience deals with the likelihood of priming CML BM cultures with GM-CSF followed by exposure to Cytarabine to evaluate Ph’c1one depletion. The BMs of 12 CML pts (3 newly diagnosed, 6 chronic phase, 3 hematological/cytogenetic complete remission) were cultured during the 24 hrs as follows: 1. controls; 2: GM-CSF (Leukomax, Schering Plough) 0.2 μ g/ml; 3. Cytarabine (Ara-C, Rontag) 0.1 μ g/ml 6 hrs before harvesting; 4. GM-CSF + cytarabine (as in 2 and 3). Colchicine 0.1 μ g/ml was added 1 hr before harvesting. Mitotic index (MI) was expressed as X ± SE for all cultures (Table 1). Table 1: Mitotic index mean values according to cultures: Culture MI (X ± SE) 1. Controls 4.50 ± 120 * * P 2. GM-CSF 6.75 ± 1.80 *≈ 3. Cytarabine 3.00 ± 0.78 4. GM-CSF + Cytabarine 3.50 ± 0.77 * p According to these data, MI in CML BMs exposed to GM-CSF Is higher than MI of controls ( * P P In vitro , more Ph’ + CML cells can be killed with cyterabine in BMs previously exposed to GM-CSF Could this experience be useful to develop new therapeutic strategies for Ph’ + CML pts?