Angiogenesis is a key factor of tumor progression. Considering, that the tumor vessels are heterogeneous and differ in morphology and clinical significance, the purpose of this research was to study of the morphological features of tumor vessels and their relationship with the clinical characteristics and morphological features of breast cancer (BC). In this pilot study the tumor samples received from 59 patients with T1–T2 stages of ductal invasive carcinomas were included. The sections were stained with hematoxylin and eosin and immunohistochemically using antibodies to CD34. The morphological features and the number of different types of tumor vessels were assessed microscopically and were compared with grade, lymph node metastasis, hormone receptors, HER2/neu status and with the presence of tumor emboli in vessels (lymphovascular invasion). We identified the following types of tumor vessels in BC: the normal microvessels, the dilated capillaries of peritumoral stroma, the atypical dilated capillaries and the “cavitary” structures (CS) type-1 and type-2 relating to the “cavitary” type of angiogenesis that was described by us earlier. The number of dilated capillaries correlated with CS type-1 (p = 0.003), CS type-2 (p = 0.002), atypical dilated capillaries (p = 0.0008) and with lymphovascular invasion (p = 0.005); the presence of atypical dilated capillaries—with CS type-1 (p < 0.00001), CS type-2 (p = 0.00004), lymphovascular invasion (p = 0.0002) and with the tumor grade (p = 0.003); the number of CS type-1—with estrogen receptor (p = 0.002) and progesterone receptor (p = 0.002) status and with lymphovascular invasion (p = 0.004); the presence of CS type-2—with positive Her2/new status (p = 0.0002) and lymphovascular invasion (p = 0.01). The density of normal microvessels was not associated with other types of tumor vessels and with clinical characteristics of BC. These data indicate that varied types of tumor vessels are associated with different morphological characteristics of BC, such as hormone receptors and HER2/neu status, lymphovascular invasion. We believe that the atypical dilated capillaries are related to the “cavitary” type of angiogenesis. The strong correlations of lymphovascular invasion with CS type-1 and atypical dilated capillaries testify that the “cavitary” type of angiogenesis may play a significant role in the formation of tumor emboli in the vessels.

The “cavitary” type of angiogenesis in patients with gastric cancer (GC) is described for the first time. Material and methods: The samples of tumour and adjacent gastric mucosa (GM) in 73 patients with GC who had undergone radical surgery were being studied. The sections were stained with hematoxylin and eosin (H&E) and immunohistochemically (IGH) using antibodies to CD34. Results: А new type of vessel formation consists of the appearance of cavitary structures (CS) in tumours and the adjacent GM, which are then lined by endothelial cells and merged into the blood vessels of the organ. We believe that the CS can be formed by means: 1) of the abruption of layers of epithelial cells (both normal and tumoral) from their underlying foundation and their desquamation into the lumen of the “obliterated” gastric glands (GG); 2) of the dilatation of the GG and thinning of their walls; 3) of the formation of “cavity” directly in the lamina propria of GM or in the tumoral stroma. It was noted that only the presence of multiple “cavitary” vessels (CV) of type-1 had been associated with the decrease of 3-year overall survival (OR=15,0, 95%CI=2,96-76,31) and relapse-free survival (OR=14,93, 95%CI=4,34-51,38). We also observed the improvement of the long-term outcomes in patients with GC having received antibacterial therapy (AT) before surgery that can be associated with its influence on the formation of CV type-1. Conclusion: The described new type of angiogenesis is of great clinical importance.

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The gut microbiota is currently considered an external organ of the human body that provides important mechanisms of metabolic regulation and protection. The gut microbiota encodes over 3 million genes, which is approximately 150 times more than the total number of genes present in the human genome. Changes in the qualitative and quantitative composition of the microbiome lead to disruption in the synthesis of key bacterial metabolites, changes in intestinal barrier function, and inflammation and can cause the development of a wide variety of diseases, such as diabetes, obesity, gastrointestinal disorders, cardiovascular issues, neurological disorders and oncological concerns. In this review, I consider issues related to the role of the microbiome in the regulation of intestinal barrier function, its influence on physiological and pathological processes occurring in the body, and potential new therapeutic strategies aimed at restoring the gut microbiome. Herewith, it is important to understand that the gut microbiota and human body should be considered as a single biological system, where change of one element will inevitably affect its other components. Thus, the study of the impact of the intestinal microbiota on health should be considered only taking into account numerous factors, the role of which has not yet been fully elucidated.

People come in contact with a huge number of nanoparticles (NPs) throughout their lives, which can be of both natural and anthropogenic origin and are capable of entering the body through swallowing, skin penetration, or inhalation. In connection with the expanding use of nanomaterials in various industrial processes, the question of whether there is a need to study the potentially adverse effects of NPs on human health becomes increasingly important. Despite the fact that the nature and the extent of damage caused depends on the chemical and the physical characteristics of individual NPs, there are also general mechanisms related to their toxicity. These mechanisms include the ability of NPs to translocate to various organs through endocytosis, as well as their ability to stimulate the production of reactive oxygen species (ROS), leading to oxidative stress, inflammation, genotoxicity, metabolic changes, and potentially carcinogenesis. In this review, we discuss the main characteristics of NPs and the effects they cause at both cellular and tissue levels. We also focus on possible mechanisms that underlie the relationship of NPs with carcinogenesis. We briefly summarize the main concepts related to the role of endogenous mineral organic NPs in the development of various human diseases and their participation in extra-bone calcification. Considering data from both our studies and those published in scientific literature, we propose the revision of some ideas concerning extra-bone calcification, since it may be one of the factors associated with the initiation of the mechanisms of immunological tolerance.