Purpose of the study. An analysis of blood levels of TGF-β, TGFR2, TNF-α, TNF-αR1, TNF-αR2, CD44 and MMP9 in patients with various biological subtypes of breast cancer receiving neoadjuvant chemotherapy.
Materials and methods. This article presents an analysis of levels of growth and progression factors (TGF-β, TGFR2, TNF-α, TNF-αR1, TNF-αR2, CD44 and MMP9) in the blood of 162 patients with various biological subtypes of locally advanced breast cancer receiving 8 cycles of neoadjuvant chemotherapy.
Results. Levels of TGF-β, TGFR2, TNF, TNF-α, TNFR1, TNFR2, CD44, MMP9 in patients with all BC subtypes were high before the treatment. After chemotherapy cycles, the values decreased statistically significantly in all BC subtypes: CD44 decreased by 25.2 %, 30 % and 54.7 % in luminal A, luminal B and TNBC, respectively; TNFα– by 26.2 %, 48.3 % and 50.8 %, respectively; TNFα-R1 – by 52.1 %, 39.2 % and 50.3 % respectively; TNFα-R2 – by 31.7 %, 32.8 % and 41.9 % respectively; MMP9 – 35.3 %, 32.6 % and 43.3 % respectively.
Conclusions. We identified a combination of growth and progression factors which determines the chemotherapy sensitivity and resistance in all subtypes of breast cancer; so, a decline in the levels of TGF-β, TNFα, MMP9 and CD44 after neoadjuvant chemotherapy predicts further remission for at least 3 years. On the contrary, stabilization or an increase of these indicators leads to the early tumor progression.

Purpose of the study. An analysis of indices of free radical oxidation and respiration of mitochondria of heart cells in a malignant process in presence of diabetes mellitus and chronic neurogenic pain in experimental animals.
Materials and methods. The study included outbred female rats (n=32) and С57ВL/6 female mice (n=84). Experimental groups of rats were: intact group 1 (n=8), control group 1 (n=8) with diabetes mellitus (DM), comparison group 1 (n=8) with standard subcutaneous transplantation of Guerin’s carcinoma, main group 1 (n=8) with Guerin’s carcinoma transplanted after 1 week of persistent hyperglycemia. Experimental groups of mice were: intact group 2 (n=21), control group 2 (n=21) with a model of chronic neurogenic pain (CNP), comparison group 2 (n=21) with standard subcutaneous transplantation of melanoma (B16/F10), main group 2 (n=21) (CNP+B16/F10) with melanoma transplanted 3 weeks after the CNP model creation. Heart mitochondria were isolated by differential centrifugation. Levels of cytochrome C (ng/mg of protein), 8-hydroxy-2'-deoxyguanosine (8-OHdG) (ng/mg of protein), and malondialdehyde (MDA) (μmol/g of protein) were measured in mitochondrial samples by ELISA. Statistical analysis was performed using the Statistica 10.0 program.
Results. DM in rats upregulated 8-OHdG by 6.3 times and MDA by 1.9 times (р=0.0000) and downregulated cytochrome C by 1.5 times (р=0.0053) in heart cell mitochondria, compared to intact values. DM+Guerin’s carcinoma in rats increased 8-OHdG by 14.0 times and MDA by 1.7 times (р=0.0000) and decreased cytochrome C by 1.5 times (р=0.0000), compared to intact values. CNP in mice did not affect the studied parameters in mitochondria of the heart. CNP+B16/F10 in mice increased 8-OHdG by 7.1 times and MDA by 1.6 times (р=0.0000) and decreased cytochrome C by 1.6 times (р=0.0008).
Conclusions. Comorbidity (diabetes mellitus, chronic neurogenic pain) together with malignant pathology aggravates mitochondrial dysfunction of heart cells with destabilization of the respiratory chain mediated by free radical oxidation processes.

Purpose of the study. Evaluation of the cytotoxic effect of strains RVK100 and RVK228 of a new unclassified group of human rotaviruses on human peripheral blood mononuclear cells in vitro.
Materials and methods. As a material for the study, we used peripheral blood mononuclear cells of a healthy donor. The cells were exposed to two strains of rotaviruses RVK100 and RVK228 for 24 and 48 hours. The cytotoxicity of the tested viruses was assessed using the Colorimetric Cell Viability Kit I (WST-8) (PromoCell, Germany). Analysis of lymphocytes subpopulation composition was assessed on a FACSCantoII flow cytometer (BD, USA) using monoclonal antibodies to human antigens: CD3, CD4, CD8, CD16/56, CD19, CD45, CD38, HLA-DR.
Results. According to the cell viability test, there was no significant decrease in the number of living cells in the samples with the addition of viruses in comparison with the control. On the contrary, after 48 hours of cultivation in the samples with the addition of RVK228, the number of living cells was significantly higher than in the control. The study of lymphocytes subpopulation composition showed a relative increase in the number of early activation markers on T cells in samples with viruses, which was also more pronounced in samples with the addition of RVK228.
Conclusion. The investigated strains of rotaviruses have no cytotoxic effect on human peripheral blood mononuclear cells. Moreover, the RVK228 strain is likely to have the ability to activate lymphocytes.

The discovery of immune checkpoint inhibition has revolutionized the treatment of many solid malignancies, including non-small cell lung cancer (NSCLC). Immune checkpoint inhibitors (ICI) can restore the antitumor immune response by blocking the inhibition of T-cell activation. Anti-programmed death-ligand 1 (PD-L1) is currently the main biomarker of the effectiveness of anti-PD-1 / PD-L1 blockade in the treatment of NSCLC without driver mutations. High tumor mutational burden suggests an increased neoantigens load and has been associated with the effectiveness of ICI therapy. Microsatellite instability, a biomarker approved for immunotherapy across solid tumors, but it is uncommon in NSCLC. Primary resistance to ICIsis characteristic of NSCLC with driver mutations, acquired is associated with immunoediting resulting in the depletion of potentially immunogenic neoantigens. The review discusses recent advances and future directions for predicting the results of immunotherapy in patients with NSCLC.

The regimens of anticancer therapy have been intensified and methods of high-dose chemotherapy (HDCT) have been introduced for recent years which made it possible to achieve significant progress in the results of tumor treatments. Intensification of chemotherapy regimens in cancer patients leads to the emergence of risk factors of invasive candidiasis (IC) development: agranulocytosis, disruption of the integrity of the mucous membranes, prolonged use of CVC, repeated antibiotic therapy, long-term parenteral nutrition. Thus, intensification of anticancer therapy may be accompanied by an increase in infection-mediated mortality.
IC is the most common invasive mycosis in Russia. More than 11 thousand cases of IC occur in our country every year. The frequency IC in Russia is 8.29 per 100 thousand of the population, which corresponds to the results of the LIFE study in European countries where this indicator varies from 2.2 to 11 per 100 thousand of the population. There are no clinical signs or symptoms specific for IC. It develops in patients with concomitant diseases, which significantly complicates the diagnosis. In this regard, an urgent issue is to improve the diagnosis of candidal infectious complications in cancer patients in order to optimize treatment by studying serological markers that have the greatest value in the diagnosis of infectious complications in cancer patients.

Cancer is one of the leading causes of death and disability worldwide. Timely diagnosis and the introduction of new effective treatments, including intensive radiation and chemotherapy regimens, have significantly improved survival forecasts in recent years. At the same time, the use of these types of treatment increases the risk of complications, one of which includes chemotoxic cardiopathies. In this regard, timely detection and treatment of complications from the cardiovascular system in patients receiving chemotherapy courses in combination with surgical methods of treatment is important. This paper presents an assessment of the significance of the use of cardiomarkers in the early diagnosis of acute myocardial infarction that developed during chemotherapy in a patient with tongue cancer with a complicated cardiac history. Patient M., 45 years old, was admitted for surgical treatment for cancer of the tongue St. IVA, T4aN1M0, cl. gr. 2. Planned laboratory and instrumental studies were performed. Contraindications for surgical treatment were not identified. A preoperative course of chemotherapy was performed, against the background of which the patient's condition worsened with symptoms of acute cardiopathy. A second ECG was urgently performed, as a result of which an increase in the ST segment in III, aVF was established, as well as a study of the concentration of cardiomarkers: highly sensitive troponin I, N-terminal propeptide of natriuretic hormone, creatine phosphokinase MB, myoglobin, the dynamics of changes in the level of which indicated the development of acute coronary syndrome. The complex application of diagnostic procedures, including the determination of the level of cardiomarkers, made it possible to timely diagnose the development of acute type 1 myocardial infarction in a patient with tongue cancer on the background of chemotherapy. When analyzing the entire array of clinical and laboratory data, the leading initiating factor that played a decisive role in the development of myocardial infarction in this case was, in our opinion, a preoperative course of polychemotherapy with paclitaxel and carboplatin, which have cardiotoxicity. Thus, the category of patients with an initial unfavorable background, due to a common malignant process and the presence of a history of cardiodisfunction, requires more careful preparation for preoperative courses of polychemotherapy, including cardiotropic therapy with mandatory monitoring of the level of the main cardiomarkers. The most significant changes were in the levels of creatine phosphokinase MB, troponin I, and myoglobin, which were recorded in the first hours of myocardial infarction. An association was found between an increase in troponin I concentration and an increase in the ST segment of the electrocardiogram.