The production of nanomaterials through environmentally friendly methods is a top priority in the sustainable development of nanotechnology. This paper presents data on the synthesis of silver nanoparticles using an aqueous extract of Sphagnum fallax moss at room temperature. The morphology, stability, and size of the nanoparticles were analyzed using various techniques, including transmission electron microscopy, Doppler laser velocimetry, and UV-vis spectroscopy. In addition, Fourier transform infrared spectroscopy was used to analyze the presence of moss metabolites on the surface of nanomaterials. The effects of different concentrations of citrate-stabilized and moss extract-stabilized silver nanoparticles on cell viability, necrosis induction, and cell impedance were compared. The internalization of silver nanoparticles into both monolayers and three-dimensional cells spheroids was evaluated using dark-field microscopy and hyperspectral imaging. An eco-friendly method for the synthesis of silver nanoparticles at room temperature is proposed, which makes it possible to obtain spherical nanoparticles of 20–30 nm in size with high bioavailability and that have potential applications in various areas of human life.

Tumor employs non-cancerous cells to gain beneficial features that promote growth and survival of cancer cells. Despite intensive research in the area of tumor microenvironment, there is still a lack of reliable and reproducible in vitro model for tumor and tumor-microenvironment cell interaction studies. Herein we report the successful development of a heterogeneous cancer-stroma sphere (CSS) model composed of prostate adenocarcinoma PC3 cells and immortalized mesenchymal stem cells (MSC). The CSS model demonstrated a structured spatial layout of the cells, with stromal cells concentrated at the center of the spheres and tumor cells located on the periphery. Significant increase in the levels of VEGFA, IL-10, and IL1a has been detected in the conditioned media of CSS as compared to PC3 spheres. Single cell RNA sequencing data revealed that VEGFA was secreted by MSC cells within heterogeneous spheroids. Enhanced expression of extracellular membrane (ECM) proteins was also shown for CSS-derived MSCs. Furthermore, we demonstrated that the multicellular architecture altered cancer cell response to chemotherapeutic agents: the inhibition of sphere formation by topotecan was 74.92 ± 4.56 % for PC3 spheres and 45.95 ± 7.84 % for CSS spheres (p < 0.01), docetaxel showed 37,51± 20,88 % and 15,67± 14,08 % inhibition, respectively (p < 0.05). Thus, CSS present an effective in vitro model for examining the extracellular matrix composition and cell-to-cell interactions within the tumor, as well as for evaluating the antitumor activity of drugs.

Determination of cancer risk factors allow us to develop diagnostics tests that improved identification and reduced the rate of mortality of most frequent cancer diseases including breast cancer, prostate cancer, gastrointestinal tumors. Today individual risk of breast cancer considers personal genetics, medical history of patient, lifestyle, and a number of additional factors. Calculation of the first mathematical models for breast cancer risk assessment included anthropometric data, hormonal status, and family history of cancer. The discovery of BRCA1 and BRCA2 genes role in the development of breast cancer and the accumulation of data from population studies contributed to the introduction of the genetic component into mathematical models. The trend of the last decade is the integration of the polygenic component into the scheme for calculating the individual risk of breast cancer. In this review, we have analyzed existing models, assessed their relevance for certain groups of patients, studied the trends in the development of methods for molecular genetic diagnosis of breast cancer and determining the personal risk of developing the disease.

CAR-T therapy has revolutionized the field of oncology, offering a promising treatment option for cancer patients. However, the significant morbidity associated with therapy-related toxicity presents a major challenge to its widespread use. Despite extensive research into the underlying mechanisms of CAR-T therapy-related toxicity, there are still many unknowns. Furthermore, the lack of adequate in vitro models for assessing immunotoxicity and neurotoxicity further complicates the development of safer cellular therapies. Previously in our laboratory, we developed cancer-stroma spheres (CSS) composed of prostate adenocarcinoma PC3 cells and mesenchymal stem cells (MSC). Herein we present evidence that multicellular CSS could serve as a valuable in vitro model for toxicity studies related to CAR-T therapy. CSS containing CD19-overexpressing PC3M cells exhibited increased secretion of CAR-T cell toxicity-associated IL-8, MCP-1, and IP-10 in the presence of anti-CD19 CAR-T cells, compared to spheres derived from single cell types.

Vascular endothelial growth factor receptor 3 (VEGFR3) assumes a pivotal role in regulating the development and maintaining the structural integrity of the lymphatic system. Decreased activity of VEGFR3 can precipitate aplasia or hypoplasia of lymphatic system components, culminating in primary lymphedema. To date, numerous genetic variants have been identified within the FLT4 gene, which encodes VEGFR3; however, the majority of these remain uncharacterised and are classified as ‘variants of uncertain significance’. In preceding investigations involving FLT4 sequence analysis conducted on individuals presenting with primary lymphedema, we identified several rare genetic variants that possess the potential to modulate the functional activity of VEGFR3, including the heterozygous variant c.3175G>C (p.A1059P). Preliminary assessments encompassing clinical characteristics, family history, and predictive computational algorithms indicated that this variant was likely pathogenic. Consequently, this study presents the results of functional evaluation of the mutant VEGFR3 activity in cell models overexpressing the FLT4 variant c.3175G>C. VEGFC-dependent VEGFR3 phosphorylation and FLT4 expression were reduced in cells with c.3175G>C FLT4 variant compared to wild-type, confirming the pathogenic role of c.3175G>C in primary lymphedema.