The tumor microenvironment (TME) is a complex and ever-changing “rogue organ” composed of its own blood supply, lymphatic and nervous systems, stroma, immune cells and extracellular matrix (ECM). These complex components, utilizing both benign and malignant cells, nurture the harsh, immunosuppressive and nutrient-deficient environment necessary for tumor cell growth, proliferation and phenotypic flexibility and variation. An important aspect of the TME is cellular crosstalk and cell-to-ECM communication. This interaction induces the release of soluble factors responsible for immune evasion and ECM remodeling, which further contribute to therapy resistance. Other aspects are the presence of exosomes contributed by both malignant and benign cells, circulating deregulated microRNAs and TME-specific metabolic patterns which further potentiate the progression and/or resistance to therapy. In addition to biochemical signaling, specific TME characteristics such as the hypoxic environment, metabolic derangements, and abnormal mechanical forces have been implicated in the development of treatment resistance. In this review, we will provide an overview of tumor microenvironmental composition, structure, and features that influence immune suppression and contribute to treatment resistance.

In recent years, there has been a surge of interest in tumor microenvironment-associated cancer vaccine therapies. These innovative treatments aim to activate and enhance the body’s natural immune response against cancer cells by utilizing specific antigens present in the tumor microenvironment. The goal is to achieve a complete clinical response, where all measurable cancer cells are either eliminated or greatly reduced in size. With their potential to revolutionize cancer treatment, these therapies represent a promising avenue for researchers and clinicians alike. Despite over 100 years of research, the success of therapeutic cancer vaccines has been variable, particularly in advanced cancer patients, with various limitations, including the heterogeneity of the tumor microenvironment, the presence of immunosuppressive cells, and the potential for tumor escape mechanisms. Additionally, the effectiveness of these therapies may be limited by the variability of the patient’s immune system response and the difficulty in identifying appropriate antigens for each patient. Despite these challenges, tumor microenvironment-targeted vaccine cancer therapies have shown promising results in preclinical and clinical studies and have the potential to become a valuable addition to current cancer treatment and “curative” options. While chemotherapeutic and monoclonal antibody treatments remain popular, ongoing research is needed to optimize the design and delivery of these therapies and to identify biomarkers that can predict response and guide patient selection. This comprehensive review explores the mechanisms of cancer vaccines, various delivery methods, and the role of adjuvants in improving treatment outcomes. It also discusses the historical background of cancer vaccine research and examines the current state of major cancer vaccination immunotherapies. Furthermore, the limitations and effectiveness of each vaccine type are analyzed, providing insights into the future of cancer vaccine development.

The basic goal of this study was to synthesize zinc oxide nanoparticles using the Chelidonium majus extract and asses their cytotoxic and antimicrobial properties. The synthesized ZnO NPs were characterized by UV-Vis, Scanning Electron Microscopy (SEM) with EDS profile, Fourier Transform Infrared Spectroscopy (FTIR), X-ray diffraction (XRD), Transmission Electron Microscopy (TEM) and Atomic Force Microscopy (AFM). The aforementioned methods confirmed that the size of synthesized ZnO nanoparticles was at the range of 10 nm. The antimicrobial activity of ZnO nanoparticles synthesized using the Ch. majus extract was tested against standard strains of bacteria (Staphylococcus aureus NCTC 4163, Pseudomonas aeruginosa NCTC 6749, Escherichia coli ATCC 25922), yeast (Candida albicans ATCC 10231), filamentous fungi (molds: Aspergillus niger ATCC 16404, dermatophytes: Trichophyton rubrum ATCC 28188), clinical strains of bacteria (Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus) and yeast (Candida albicans). The study showed that zinc oxide nanoparticles were excellent antimicrobial agents. What is more, biologically synthesized ZnO nanoparticles demonstrate high efficiency in treatment of human non-small cell lung cancer A549.

So far, a protective influence of phytosterols on the human organism and atherogenesis has been suggested. Most studies have concentrated on the cytotoxic efficacy of phytosterols on cancer cells. However, there are only a few reports showing their influence on normal cells. The aim of the present study was to determine whether dietary plant sterols and their thermal processing products could influence the viability of normal, abdominal endothelial cells that play a crucial role in atherogenesis. Thus, we studied the effect of rapeseed oil-extract components, β-sitosterol, cholesterol and their epoxy-derivatives, 5α,6α-epoxy-β-sitosterol and 5α,6α-epoxycholesterol, on the proliferation and viability of human abdominal aorta endothelial cells HAAE-2in vitro. We showed strong cytotoxic properties of β-sitosterol in HAAE-2 cells (half maximal inhibitory concentration (IC₅₀) = 1·99 (sem0·56) μm) and, interestingly, a weaker cytotoxic effect of 5α,6α-epoxy-β-sitosterol (IC₅₀>200 μm). Moreover, we observed a significantly stronger cytotoxic activity of β-sitosterol than cholesterol (IC₅₀ = 8·99 (sem2·74) μm). We also revealed that β-sitosterol as well as cholesterol caused apoptosis, inducing caspase-3 activity in the cells (60 % increase compared with control cells) that corresponded to the DNA fragmentation analysis in a terminal uridine deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling (TUNEL) study. Although absorption of plant sterols is low compared with cholesterol, they can still influence other physiological functions. Since they effectively reduce serum LDL-cholesterol and atherosclerotic risk but also decrease the viability of cancer cells as well as normal cells in a time- and dose-dependent mannerin vitro, their influence on other metabolic processes remains to be elucidated.