ATTACHMENT OF CHRONIC LYMPHOCYTIC LEUKAEMIA CELLS BY AUTOLOGOUS POLYMORPHONUCLEAR NEUTROPHILS MEDIATED BY BISPECIFIC ANTI-CD19/CD64 ANTIBODY.

Chronic lymphocytic leukemia (CLL) is the most common adult leukaemia in the US and in Europe, including Georgia. CLL presents with clonal expansion and accumulation of CD5+CD19+CD23+ cells in peripheral lymphoid organs and tissues and in bone marrow. The disease remains incurable, albeit there are new molecular and immunotherapy methods currently available, which, in conjunction with chemotherapy, lead to the "precision therapy" approach.

DETERMINING THE RISK OF THROMBOSIS AMONG THE PATIENTS WITH ESSENTIAL THROMBOCYTHEMIA.

The aim of the studywas to determine the risk of thrombosis among patients with Essential thrombocythemia based on the modern criteria of diagnosis and to reveal the treatment accordingmethods of research in Georgia. We analyzed clinical manifestations of 25 cases of Essential thrombocythemia diagnosed in 2013-2017 y. at the Institute of Hematology and Transfusiology.

THE PROGNOSTIC SIGNIFICANCE OF COMBAIND EXPRESSION OF ZAP-70 AND CD38 IN CHRONIC LYMPHOCYTIC LEUKEMIA.

Our aim was to assess the inter links of the markers CD38 and ZAP-70 based on our materials, the attitude according to the disease stage, and to document which of them had leading meaning for prognosis and treatmend of the disease. In our study we have used flow cytometry for detection CD38 and ZAP-70+ markers expression. (58 patients to assessments their prognostic value in сhronic lymphocytic leukemia (CLL), Correlation to Rai stages and relationships between this markers and outcome of therapy).

CHRONIC MYELOID LEUKEMIA EXPECTED RELAPSE'S CLINICAL-LABORATORY INDEXES.

Today Chronic Myeloid Leukemia (CML) relapse's final assessment and monitoring in the whole world is implemented by BCR-ABL gene quantitative detection - during the polymerase chain reaction (by PSR means). Implementation of this monitoring materially and technically is not often available and remission during years is being assessed using monthly clinical-laboratory data. Proceeding from this, the goal of our work was to find the clinical-laboratory features, indicating the expected relapse and require the urgent molecular research carry out.

Correlation of the expression of CD32 and CD180 receptors on CLL cells and MEC1 cell line.

Chronic Lymphocytic Leukemia (CLL) presents with clonal expansion and accumulation of CD5+CD19+CD23+ cells in peripheral lymphoid organs and tissues and in bone marrow. CLL is supposedly driven by exogenous and/or endogenous (auto)antigen(s) and there is increasing evidence that CLL cells receive microenvironmental signals which support their growth, survival and expansion in vivo. We have previously shown that powerful signals are received by CLL cells through CD180 orphan toll-like receptor.

Aberrant expression of Fcγ-receptors and Toll like receptor CD180 on monocytes from patients with chronic lymphocytic leukaemia.

Chronic lymphocytic leukemia (CLL) is the most common leukaemia in the US and in Europe, including Georgia. Patients with CLL are susceptible to infectious diseases as a result of both, the disease progression and chemotherapy that indicates deficiency of immune responses to pathogens, including innate immunity, mediated by monocytes. Monocytes are also often recruited by monoclonal antibodies (mAbs) which express anti-tumour toxicity through Fcγ-receptor (FcγR)-mediated phagocytosis of opsonised leukaemic cells.

Phase I study of quizartinib administered daily to patients with relapsed or refractory acute myeloid leukemia irrespective of FMS-like tyrosine kinase 3-internal tandem duplication status.

Purpose: FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) mutations in acute myeloid leukemia (AML) are associated with early relapse and poor survival. Quizartinib potently and selectively inhibits FLT3 kinase activity in preclinical AML models.

Patients And Methods: Quizartinib was administered orally at escalating doses of 12 to 450 mg/day to 76 patients (median age, 60 years; range, 23 to 86 years; with a median of three prior therapies [range, 0 to 12 therapies]), enrolled irrespective of FLT3-ITD mutation status in a phase I, first-in-human study in relapsed or refractory AML.