We used the bortezomib plus dexamethasone (VD) and bortezomib plus MP (VMP) in 56 previously untreated elderly patients with multiple myeloma. The patients were 65–89 years old. For patients who received bortezomib plus MP the overall response rate was 83%. 33.3% of patients achieved complete response (near-complete response + complete response) (based on EBMT criteria). For patients who received bortezomib plus dexamethasone the overall response rate was 73%. 34.6% of patients achieved complete response. Median overall survival in patients treated with bortezomib plus dexamethasone and bortezomib plus MP has not been reached. Median event-free survival was 15 and 17 months respectively. Side effects of bortezomib were predictable and manageable. The most common adverse events reported were asthenia, neuropathy, neutropenia and anemia. Serious adverse events were rare. These results establish VMP and VD as modern strategies in therapy of elderly untreated patients with multiple myeloma. VMP and VD is highly effective and well tolerated in elderly patients (> 65 years) with newly diagnosed multiple myeloma.

   The aim of the study was to analyze the etiologys of infectious complications (especially the role of respiratory viruses in patients with haematological malignancies).

   The supervised patients were divided into two subgroups: the first was patients with hemoblastosis and clinically evidence of infectious complications (n = 50), and the second – patients without clinical features of infection (control group) (n = 35). We analyzed the pharyngeal flora of patients by means of bacteriological and mycological methods and the frequency of respiratory viruses (Respiratory syncytial virus, Influenza A and B, Parainfluenza – 1, 2, 3, 4, rhinoviruses, adenoviruses, coronaviruses, metapneumovirus, bocavirus); herpesviruses (herpes simplex type 1 and 2, herpes type 6, Epstein-Barr virus and Cytomegalovirus), Mycoplasma pneumoniae and Chlamydophila pneumoniae by means of PCR. Respiratory infections were detected in 62 % in subgroup with clinically evidence of infectious complications and only in 22.8 % in the second subgroup. In many cases herpesvirus infection (Epstein-Barr virus and Cytomegalovirus) was associated with respiratory viral infections. So, respiratory and herpes viral infections must be carefully controlled in immunosuppressed patients with hematological malignancies.

   Cytomegalovirus infection (CMV) is an extremely serious problem in patients after hematopoietic stem cells transplantation (HSCT). We have evaluated importance of major risk factors CMV development in patients after allogeneic HSCT (n = 168) from related (n = 56), unrelated (n = 90) or haploidentical donors (n = 22). Clinical importance of HSCT type as risk factors CMV development was shown; patients after unrelated or haploidentical HSCT had the worst prognosis. We also demonstrated that ≥ 2 grade acute GVHD statistically significant increase CMV reactivation probability after any types of HSCT. Comparison of infection reactivation frequency and event-free survival between subgroups of patients, received HSCT from CMV-positive and CMV-negative donors, absence of any differences was revealed. In the second group CMV infection was more severe. Preventive gancyclovir treatment has not shown efficacy and any influence on frequency of CMV reactivation.

   Osteopetrosis (“Marble disease”) – is a group of diseases characterized by inability of osteoclasts to resorb the osteal tissue that leads to increased bone fragility, despite density increase. Analysis of data of 27 patients with infantile (malignant) autosomal recessive osteopetrosis (ARO) (21 boys and 6 girls) allowed to describe and summarize the basic clinical features: hematopoiesis suppression, liver and spleen enlargement, vision and hearing failure, delay of psychomotor development, other neurological symptoms, specific radiological bone changes.

   In present study influence of allogeneic bone marrow mesenchymal stem cells (MSC) on patients’ leukemic cells is investigated. Influence on in vitro sensitivity to antileukemic drugs and spontaneous and cytarabine-induced apoptosis of leukemic cells was studied. It has`been shown that MSC reduce myeloid leukemic cells sensitivity to daunorubicine. However, MSC did not statistically significant influence on spontaneous and cytarabine-induced apoptosis of leukemic cells.

   A lymphocyte lineage which is referred to as NKT cells expresses both markers of NK cells and T lymphocytes. NKT cells play a key role in the regulation of different types of immune responses, contribute to the protection from tumor growth and metastasis, from different intracellular infections and from development of autoimmune diseases. NKT cells are of vital importance in the induction of antitumoral immune response due to their production of IFN-γ which activates NK cells, CD8+ T lymphocytes and macrophages.

   The journal begins to publish a series of lectures for doctors, which is devoted to the molecular mechanisms of leukemia. Modern medicine is on the verge of the emergence of a large number of new generation drugs whose activity is aimed at modulating (activating or suppressing) the functions of certain target molecules that are involved in the processes of leukemia. Such targets can be enzymes, proteins with other (non-enzymatic) functions, genomic DNA, mRNA, or, for example, certain lipid components of cell membranes. It can be expected that such targeted (targeted) therapy will significantly improve the results of the treatment of hematological tumors. However, its application will make fundamental changes in the work of an oncologist. This is due to the fact that rapidly improving methods of molecular diagnostics will make it possible in the near future to detect in patients not only specific for this type of tumor (recurrent) genetic aberrations, but a whole range of genomic disorders. And since the evolution of each specific tumor proceeds according to an “individual” program, there is a high probability that the combination of various aberrations in leukemia cells will also have an individual (patient-specific) character. If at the same time the doctor has a whole set of targeted drugs “at hand”, then this will require him to be able to independently draw up an individual course of therapy for each patient. Therefore, the hematologist must understand the cellular processes, the action of which he is going to modulate with the help of such drugs. For example, to know which of them can and should be used together, and for which drugs the combined use is meaningless or even harmful. In a short series of lectures it is impossible to consider the most important issues of molecular biology and genetics, but the author does not set himself such a task. It is much more important to teach the physician to understand the key mechanisms of interactions between various cellular molecules and how these interactions are disrupted in the presence of oncogenic proteins. There are many tumor-causing target molecules, and the number of mechanisms by which they realize their pathological potential is not so big. Therefore, in the first lectures, the main molecular mechanisms, the disruption of which most often leads to the development of leukemia, will be considered. In subsequent lectures, the main genetic aberrations characteristic of hematological tumors of myeloid and lymphoid origin, as well as targeted drugs used in the treatment of these diseases, will be described. Today there is a large amount of literature on the issues under discussion, we will give links to published reviews, giving preference to works that are in the public domain. Internet access. As a “basic” source, a series of lectures by E.  B. Vladimirskaya “Mechanisms of hematopoiesis and leukemogenesis” published 3 years ago [1] is used, so questions that covered in detail in this work, will not be considered here. Since many references will be given to English-language literature, in this series of lectures widely used international names for proteins and genes will be used, and English names of the main terms will be given, abbreviations will be deciphered and the origin of the names will be explained (where necessary and possible). As an introduction to the etymology of gene names, the material given in Appendix 1 can be considered.