Monocytes and macrophages play an important role in the development of inflammatory diseases, including sepsis, etc. In addition to their role as “scavengers,” macrophages secrete various substances (mainly cytokines and chemokines), which have a systemic effect and modulate the microenvironment of the inflammatory focus. Disruption of their normal function can cause various immune pathologies and changes in tissue homeostasis. Macrophages are able to transmit signals to other cells in the area of inflammation, including various cytokines and other compounds. Usually, they are secreted directly into the extracellular space. However, the lifetime and range of action of these substances may be limited. An alternative method of intercellular communication is the packaging of substances into extracellular vesicles, which can help in signal propagation. Extracellular vesicles are small particles with a bilayer lipid membrane that transport various biologically active substances. There are different types of extracellular vesicles, each of which can have its own specific effect on other cells. Due to the presence of specific receptors on the surface of the vesicles, they can make selective delivery of biological molecules to certain cells. Vesicles can contain various components, such as nucleic acids, proteins, lipids, and even individual cell organelles. Therefore, it is not surprising that vesicles are able to modulate physiological processes in the body and be involved in the pathogenesis of various diseases. Establishing the mechanisms of vesicle participation in the development of inflammatory diseases, including chronic ones, is extremely important. The aim of the present study was to determine whether extracellular vesicles are capable of modulating the immune response. To do this, we assessed cytokine secretion by macrophages treated with vesicles from LPS-stimulated monocytes and macrophages. It was found that cells that received vesicles from LPS-activated monocytes and macrophages secrete more pro-inflammatory signaling molecules: the cytokine IL-6 and the chemokine IL-8. The results demonstrate that intercellular interaction and transmission of the inflammatory signal of monocytic cells also occurs through extracellular vesicles. In the future, additional research is needed to understand the full picture of what substances in the extracellular vesicles of monocytes and macrophages allow them to have an immunomodulatory effect not only on each other, but also on other types of cells.

The COVID-19 pandemic caused by the SARS-CoV-2 coronavirus remains a global public health concern due to the systemic nature of the infection and its long-term consequences, many of which remain to be elucidated. SARS-CoV-2 targets endothelial cells and blood vessels, altering the tissue microenvironment, its secretion, immune-cell subpopulations, the extracellular matrix, and the molecular composition and mechanical properties. The female reproductive system has high regenerative potential, but can accumulate damage, including due to SARS-CoV-2. COVID-19 is profibrotic and can change the tissue microenvironment toward an oncogenic niche. This makes COVID-19 and its consequences one of the potential regulators of a homeostasis shift toward oncopathology and fibrosis in the tissues of the female reproductive system. We are looking at SARS-CoV-2-induced changes at all levels in the female reproductive system.

COVID-19 pandemic was caused by SARS-CoV-2, a novel virus from the family Coronaviridae, firstly identified in Wuhan, China in 2019. COVID-19 remains one of the main challenges of healthcare, given growing numbers of people with COVID-19 in anamnesis, and given the long-lasting consequences and complications of this disease. Cancer is one of the most common diseases in the world, thus a big part of the population is affected by both COVID-19 and cancer. In this succinct review we refer to several recent works expressing a view that COVID-19 might be oncogenic, and describe molecular mechanisms of such phenomena. Next, we describe several tumorigenic changes in the tissue microenvironment as COVID-19 sequelae, which can potentially affect cancer pathogenesis and response of a tumor to therapy. 3D cell culture models are a “golden standard” of in vitro studies in translational oncology. To the best of our knowledge, 3D cell culture systems to study tumor behavior in the tissue microenvironment affected by COVID-19 have not been developed yet. We propose several actionable steps which can be taken to modify existing 3D cell culture models accordingly, to address the needs of translational oncology in the COVID-19 post-pandemic times.

The purpose of the study was to summarize and analyze modern data about non-invasive methods of molecular diagnosis and approaches to the personalized therapy of diffuse midline glioma (DMG). Material and Methods . The search and analysis of publications was carried out using Google Scholar, Pubmed, Elsevier, Web of Science, Elibrary systems. The review includes publications published from 2011 to 2022. Of the 102 articles found, 59 were used to write the review. Results . In this review, we discuss the spectrum of somatic driver mutations present in DMG tumor cells and their relationship with the sensitivity of tumor cells to certain types of therapy - a pharmacogenetic approach to the selection of individual treatments (targeted therapy). We provide examples of new methods of targeted therapy for DMG, which are currently at the stage of preclinical laboratory development. Also, we discuss examples of the use of 3D cell cultures for the development of targeted therapies, including the use of perfusion systems. The review describes the methods of analysis of liquid biopsy, which allow the detection of tumor-specific biomarkers in the non-invasive diagnosis of DMG, including a number of methods that have not yet been tested in the clinic. The following is a list of tumor-specific biomarkers for diagnosing, monitoring, and selecting targeted therapy for DMG. Finally, we discuss the possibility of implementing these methods in the clinic and present the results of several clinical trials. Conclusion . In oncology, new methods of molecular genetics, such as analysis of liquid biopsy, allow diagnosis and monitoring of treatment in cases where classical methods that require tissue sampling are not applicable (for example, the analysis of genetically heterogeneous tumors and tumors of surgically inaccessible localization). These tumors include DMG, a primary brain tumor most common in children. The available data confirm the relevance of the search for new specific tumor biomarkers, as well as targets for targeted therapy of the paediatric-type diffuse gliomas.

The transforming growth factor beta (TGF-β) signaling pathway plays complex role in the regulation of cell proliferation, apoptosis and differentiation in breast cancer. TGF-β activation can lead to multiple cellular responses mediating the drug resistance evolution, including the resistance to antiestrogens. Tamoxifen is the most commonly prescribed antiestrogen that functionally involved in regulation of TGF-β activity. In this review, we focus on the role of TGF-β signaling in the mechanisms of tamoxifen resistance, including its interaction with estrogen receptors alfa (ERα) pathway and breast cancer stem cells (BCSCs). We summarize the current reported data regarding TGF-β signaling components as markers of tamoxifen resistance and review current approaches to overcoming tamoxifen resistance based on studies of TGF-β signaling.

Hormone-receptor positive breast cancer is the most common molecular subtype and represents 60–75 % of all breast cancers (BC). The presence of specific molecular targets such as the estrogen/progesterone receptor determines the use of hormone therapy for patients with this subtype. Tamoxifen, a selective estrogen receptor modulator, remains the first adjuvant treatment choice for the hormone-receptor positive BC patients. However, tamoxifen resistance is the major limitation of its efficacy. In this regard, the study of drug resistance mechanisms as well as search for biological prognostic markers of tamoxifen efficacy is very important. Cyclin D1 is a representative of the regulatory protein family, which plays a central role in the cell cycle regulation. The data on the association between cyclin D1 and estrogen-dependent signaling as well as the characteristics of CCND1 gene and its most studied polymorphic loci, were presented. The prognostic significance of cyclin D1 in hormone-receptor positive BC receptor-positive breast cancer was described. The experimental and clinical studies data on the association between the cyclin D1 expression level and tamoxifen efficacy are analyzed. Current approaches to overcoming hormone resistance based on cyclin D1 studies were considered.