Expression of Ki-67 and CD34 on blood and bone marrow cells of CML patients with different response to imatinib and nilotinib therapy.

Aim: To assess the expression of Ki-67 protein and CD34 antigen on peripheral blood (PB) and bone marrow (BM) cells in chronic myelogenous leukemia (CML) patients with different response to tyrosine kinase inhibitors (TKI) imatinib (IM) and nilotinib (NI) therapy.

Patients And Methods: BM aspirate and PB samples from 41 CML patients treated with IM and NI were studied by cytogenetic, molecular genetic, and flow cytometry methods. According to the response to TKIs, the patients were distributed into the optimal response, warning, and treatment failure groups.

[THE STUDY OF RESPONSE TO TYROSINE KINASE INHIBITORS THERAPY IN PATIENTS WITH CHRONIC MYELOID LEUKEMIA DEPENDING ON SOCAL SCORE].

The study included 426 patients with CML in chronic phase treated with imatinib. The level of response to therapy was assessed according to the recommendations of the European Leukemia Net. Socal score determined at the beginning of the disease and was calculated by the appropriate formula.

Mechanisms of resistance in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors.

Up to date, two major mechanisms have been proposed as an explanation for myeloid cells expansion in chronic myeloid leukemia (CML). One is a reduced susceptibility of hematopoietic stem or progenitor cells to apoptosis, while the other one is an increased activity within the hematopoietic progenitor cell population. The aim of the study was to identify specific features of functional activity, proliferation rates and differentiation potential of CML hematopoietic progenitor cells of patients treated with tyrosine kinase inhibitors (TKI) by identifying number of Ki-67, Bcl-2 and CD34 positive cells in bone marrow, as well as in vitro colony-forming unit assay in patients with different response to the TKI therapy.

Functional activity of CD34-positive cells in chronic myeloid leukemia patients with different response to imatinib therapy.

Introduction: It is believed that the reason of the leukemic clone cell resistance to treatment with tyrosine kinase inhibitors during chronic myeloid leukemia (CML) is mutations in the genome of an early bone marrow progenitor cells that are CD34-positive. Such cells, regardless of treatment, acquire ability to proliferation and differentiation. This leads to the re-expansion of the CD34(+) cells.

Determination of the optimal chemotherapy drugs pretreatment time through cultivation of hemopoietic cells in CML-patients treated with tyrosine kinase inhibitors.

Background: Targeted therapy drugs, including imatinib, are used for inhibiting the marker oncoprotein of chronic myeloid leukemia - BCR-ABL tyrosine kinase. However, in some patients the drug resistance can emerge too rapidly and a previous treatment with chemotherapy drugs can lead to formation of resistance.

Aim: To evaluate the influence of drugs that were used prior to the imatinib on the performance of the functional activity of bone marrow cells from chronic myeloid leukemia patients and their individual responses to therapy.

[Change in hemograms as a predictor for developing hematologic diseases in liquidators of the accident at Chernobyl Atomic Energy Station, also having hemocirculatory disorders].

A comparative analysis was performed of hemogrammes in 134 liquidators of the Chernobyl accident with hemocirculatory disorders, in 69 non-irradiated patients presenting with like processes, in 18 patients with chronic lymphoid leukosis, and in 32 healthy subjects to determine the degree of risk for development of hematologic diseases. The risk was at its highest for thrombocytopenia and neutropenia which are laboratory signs of chronic lymphoid leukosis. The incidence of thrombocytopenia in the irradiated subjects is 4.