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It is considered that hypercholesterolemia is life-threatening and low cholesterol levels are a positive factor. However, taking into consideration the fact that cholesterol plays a key role in cell proliferation, it should be remembered that its low blood level may be linked to high cholesterol demands from neoplastic cells. The literature review analyzes the results of recent investigations of lipid metabolism in patients with hematologic cancers and their other types. All given investigations show a significant reduction in the serum levels of total cholesterol and high-density lipoproteins in patients with hematological disease at its onset. The data for other indicators of the lipid transport system are ambiguous. Such changes have been elucidated to be associated with the accumulation of cholesterol in the leukemia cells due to enhanced synthesis de novo, a more active absorption from circulation and blocked release of its surplus. If the disease runs a favorable course, lipid metabolic parameters become normalized and, in case of remission, correspond to those seen in healthy individuals. They continue to decline in patients with disease progression. This allows the consideration of cholesterol, its fractions, and apolipoproteins as biochemical prognostic markers in hematological cancer patients and as indicators for assessment of treatment results. In addition, there is evidence for the effect of chemotherapeutic agents on lipid metabolism. Recent attempts to elaborate new treatment strategies, by using the current knowledge on the role of lipid metabolism in cancers, are considered.

Aim. To study the pattern of complex chromosome damages (CCD) in acute leukemias (AL) and their place in the development of post-transplant recurrences (PTR) of AL. Materials and methods. Cytogenetic and partially molecular biological studies of bone marrow cells were conducted in 10 patients with PTR. Of them, 6 patients were diagnosed as having acute lymphoblastic leukemia (ALL), including T-ALL and Ph-positive ALL in 2 and 4 patients, respectively; and 4 patients had acute non-lymphoblastic leukemia (ANLL), including one case secondarily induced by previous polychemotherapy (PCT) and irradiation. The standard G-band staining technique complemented by multicolor fluorescence in situ hybridization in one of the cases was used. Results. It was shown that CCD had the similar pattern in 4 patients before transplantation and in PTR, progressed in 4 more patients, was absent or unnoticed in the early stage of the disease. The other recurrent chromosomal abnormalities that are worthy of notice are as follows: a) the presence of two Ph chromosomes in the cells of two of the 4 patients with Ph+ ALL; b) the frequent involvement of chromosome pairs 9, 19, 5, and 7 into the numerical and structural rearrangements. Conclusion. The important feature of PTR of AL is cellular CCDs, a portion of which is clearly related to previous PCT and may be of pathogenetic value for the development of recurrences.

Aim. To perform a dynamic study of Β-endorphin, hypoxia-inducible factor-1α (HIF-1α), and cytokines in hematologic patients. Subjects and methods. Fifty-nine patients with different types of acute leukemia (AL), 30 with anaplastic anemia (AA), 24 with thrombocytopenic purpura, and 20 healthy volunteers were examined during their 40-day stay at 3200 m above sea level. Β-Endorphin and HIF-1α were measured by a sandwich-type enzyme immunoassay using the Abcam antibodies. Cytokines (interleukin (IL)-2, IL-6, and tumor necrosis factor-α) were estimated by enzyme immunoassay applying the Pro Con kits (Saint Petersburg). Results. Serum Β-endorphin concentrations were 1.5-2-fold above the normal values in the majority of patients with AL. The patients with initial leukocytosis at onset of disease were noted to have elevated white blood cell Β-endorphin concentrations up to 85.9±22.4 pg/ml; moreover, during chemotherapy this index increased about two times (170.74±33.8 pg/ml). There was a direct correlation between the concentrations of Β-endorphin and HIF-1α (r = 0.9) and an inverse correlation between the levels of IL-6 and Β-endorphin (r = -0.7). On ascending to 3200 m, under the conditions of hypoxic hypoxia the patients with AA or idiopathic thrombocytopenic purpura showed a considerable increase in serum Β-endorphin concentrations, mainly in the acute period of being at high altitudes. Conclusion. Stress factors (tumor, use of cytostatics, pain, anemia, hypoxia, high environment temperature) stimulate the elaboration of Β-endorphin, particularly in the white blood cells of patients with AL during chemotherapy. The highest elevation in the index was seen during acute adaptation to hypoxic hypoxia.

Aim. To study the deposition of donor platelets (DP) in myelosuppressive thrombocytopenia (TP) in patients with acute leukemia (AL) or lymphosarcoma (LSA), by using a radionuclide label (51Cr) for DP. Subjects and methods. Complex clinical, hematological and radionuclide studies were conducted in 63 patients divided into 3 groups: 1) 7 healthy volunteers (a control group); 2) 37 patients with AL; 3) 19 patients with LSA. Results. Changes were found in the deposition of labeled DPs used to prevent and treat hemorrhagic syndrome in myelosuppressive TP in patients with AL or LSA. In AL, this function was established to be virtually completely suppressed whereas in LSA, some functional activity of mononuclear phagocytes was preserved. Different degrees of suppression of this function were probably related to the nature of these diseases and particularly due to varying degrees of leukemic infiltration of depot organs. A mechanism for increased consumption of transfused DP in profound TP, one of the causes of which is the myelosuppression as a result of programmed polychemotherapy, cannot be ruled out. Conclusion. By and large, the radionuclide labeling technique for DP may be useful in specifying a number of uncertain mechanisms for derangements of the thrombocytic component of hemostasis in oncohematologic diseases.

Aim. To analyze the causes of prolonged hematopoietic tissue aplasias in patients with acute leukemias (AL) after chemotherapy courses. Materials and methods. Data on 7 patients with acute myeloid leukemia, followed up at the Hematology Departments, Hematology Research Center, Russian Academy of Medical Sciences, over the period 2003 to 2007, who had developed deep bone marrow aplasia (BMA) inadequate to cytostatic drug exposure during chemotherapy, were analyzed. The authors compared in all the patients the values of peripheral blood and bone marrow (BM) puncture specimens and the results of blood tests using the polymerase chain reaction at different AL development stages with the results of an immunohistochemical study using the markers of viruses of hepatitis C and B, a herpes group (EBV, CMV, HSV-1, HSV-2) and parvovirus B19. Results. The marker of hepatitis C was detected in 6 of the 7 patients with prolonged BMA; 3 of these 6 patients showed a simultaneous infection with hepatitis B. Six of the 7 patients were found to have concomitant BM lesion with various herpes group viruses. Two patients had a resistant form of AL. Conclusion. Hepatitis C virus infection in patients and the resistant form of the disease were the principal causes of the development of BMA inadequate to cytostatic drug exposure. Affliction of abundant bone marrow cells with herpes group viruses was not a direct cause, but might substantially aggravate BMA.