No abstract

Background: Currently the main potential treatment for chronic myeloid leukemia (CML) blast phase (BP) are tyrosine kinase inhibitors. The aim of our study is to try to find any therapy in TKI resistant patients in CML BP. Material and methods: The patients were 5 male and one female (age range from 28 to 45 years old). 4 patients progressed to BP from chronic phase (CP), there was rapid progression from AP in other two pts (4 lymphoid, 1 myeloid, 1 undifferentiated). The pts were unresponsible to one or two second generation TKI treatment in BP (dasatinid, nilotinib). Two patients were also failed to respond to high dose cytarabine and methotrexate treatment after TKI failure. Chemotherapy «FLAG» (fludarabine, cytarabine high dose, G-CSF) was used to induce of CP. Results: Five of six pts achieved the second CP and deep response (1- CcyR, 3- MMR, and one BCR/ABL reduction to 0,371%).Two of these pts obtained deep response (CCyR, and bcr/abl reduction to 0.371% after unsuccessful treatment with dose mono cytarabine and methotrexat treatment. The response was short, the longest MMR duration is 48 days (patient is being prepared for ASCT). Conclusion: FLAG can induce deep molecular responses in BP pts resistant to TKIs. This regimen seems to be more effective than HDAC and HD MTX. The response is of short duration. Thus, in case of absence of relative sibling, haploidentical ASCT with unmanipulated bone marrow and posttransplantation cyclophosphamide could be the optimal treatment choice. The protocol for FLAG induced remission followed haploidentical ASCT is prepared. Disclosures No relevant conflicts of interest to declare.

4286 AML M-4 with >30% bone marrow myeloblasts was detected in 63 y old woman 2 mo after a diagnosis of chronic myelomonocytic leukemia (CMMLgrade 2). Cytogenetics showed 46, XX, del(5)(q12 q14) (N=4)/46, XX (N=18). Immune-phenotyping showed CD34+ CD117+ CD13+ CD33+ CD38+ HLADR+ CD2+. Leukemia cells were negative for inv (16), BCR/ABL, NPM, TEL/AML1, MLL/AF4, PML/RARA and AML1/ETO. She was RBC-transfusion-dependent. Therapy with cytarabine and daunorubicin and later with FLAG was ineffective and bone marrow myeloblasts increased to >70% with severe granulocytopenia and infection including pulmonary aspergillosis. She then received lenalidomide, 10 mg/d for 21 d every 4 w Bone marrow myeloblasts decreased to about 20% and granulocytopenia resolved. RBC-transfusion–dependence decreased. Cytogenetic and FISH-testing showed no detectable cells with del(5). This has persisted for 5 mo. Disclosures: Off Label Use: Lenalidomide for the treatment of AML with 5q- deletion.

The aim of our study was to compare different regimes of hematopoietic stem cell (HSC) mobilization, i.e., cyclophosphamide combined with granulocyte colony-stimulating factor (Cy/G-CSF), versus cytarabine with G-CSF (Ara-C/G-CSF). Efficiency and toxicity of these treatment regimens were assessed. Achievement of partial remission of the disease was sufficient for successful mobilization. CD34+ cell numbers in the blood showed a significant correlation with total number of CD34+ yielded by apheresis on the same day. When comparing the two groups of mobilization we have revealed that the patients treated with AraC + G-CSF yielded higher amounts of CD34+ cells in peripheral blood on the first apheresis day. Moreover, lesser occurrence of toxicity was revealed in group of patients treated with AraC-G-CSF.

A joint conference of clinicians from M.D. Anderson Medical Center (Houston, Texas, USA) and specialists from leading Russian hematological centers took place in St. Petersburg on June 30-July 1, 2017. A series of special sessions was dedicated to current issues of diagnostics and pathogenetic molecular classification in hemato-oncology, including chronic lymphocytic leukemia (CLL), acute leukemias (AL), aplastic anemias (AA), myelodysplastic syndrome (MDS), malignant lymphomas. Standard treatment schedules, as well as clinical effects of newly developed targeted drugs and combined therapeutic approaches were analyzed, with a focus on Hodgkin's disease, chronic lymphocytic and myeloid leukemias and multiple myeloma. Recent developments in AL treatment, especially, in acute myeloblastic leukemia, were also presented. Current position of hematopoietic stem cell transplantation as a curative treatment in some leukemia/lymphoma settings, opportunities for tumor immunotherapy (e.g., CART cells) and appropriate technologies were also discussed.