Background: Patients with colorectal cancer (CRC) have anemia often present as a consequence of chronic bleeding from tumor. The exact role of lL-33, Galectin-l and IL-l in the pathological genesis of anemia in colorectal cancer patients has not been elucidated yet. The main goal of this research was to analyze Gal-l, IL-l and lL-33 systemic values in anemic and non-anemic CRC patients. Methods: Concentrations of IL-33, Galectin-1 and IL-1 have been studied in blood samples of 55 CRC patients (27 without anemia and 28 with anemia). Results: CRC patients with anemia had more severe and local advanced disease compared to CRC non-anemic patients. Anemia positively correlated with higher nuclear grade, lymph and blood vessel invasion, as well as with higher TNM stage, detectable metastatic lesions in lung and liver and peritoneal carcinomatosis. Significantly higher IL-33, Gal-1 and IL-1 concentration have been found in sera of patients with CRC and detected anemia. CRC patients mostly had microcytic anemia, while ferritin values were in normal range. Analysis revealed positive mutual correlation between serum values of galectin-1, IL-1 and IL-33 in CRC patients. Level of hemoglobin negatively correlated with serum IL-33, Gal-1 and IL-1. We have analyzed the Receiver Operating Characteristic (ROC) curves of serum IL-33, Gal-1 and IL-1 showed that these cytokines can be treated as additional markers for anemia of inflammation in CRC patients. Conclusions: Predomination of Galectin-1, IL-1 and IL-33 in anemic CRC patients implicates on their potential role in anemia genesis and further development.

Galectin-3 (Gal-3) plays a multifaceted role in the development, progression, and prognosis of pancreatic ductal adenocarcinoma (PDAC). This review offers a comprehensive examination of its expression in PDAC, its interaction with various immune cells, signaling pathways, effects on apoptosis, and therapeutic resistance. Additionally, the prognostic significance of serum levels of Gal-3 is discussed, providing insights into its potential utilization as a biomarker. Critical analysis is also extended to the inhibitors of Gal-3 and their potential therapeutic applications in PDAC, offering new avenues for targeted treatments. The intricate nature of Gal-3’s role in PDAC reveals a complex landscape that demands a nuanced understanding for potential therapeutic interventions and monitoring.

Number of sclerotic glomeruli increases during the aging process. Consequently, majority of remained nonsclerosed glomeruli become hypertrophic and some of them sclerotic, too. The aim of this study was to quantify the size and connective tissue content of nonsclerosed glomeruli and to evaluate the percentage of hypertrophic ones in examined human cases during the aging. Material was right kidney's tissue of 30 cadavers obtained during routine autopsies. Cadavers were without previously diagnosed kidney disease, diabetes, hypertension, or any other systemic disease. Tissue specimens were routinely prepared for histological and morphometric analysis. Images of the histological slices were analyzed and captured under 400x magnification with digital camera. Further they were morphometrically and statistically analyzed with ImageJ and NCSS-PASS software. Multiple and linear regression of obtained morphometric parameters showed significant increase of glomerular connective tissue area and percentage. Cluster analysis showed the presence of two types of glomeruli. Second type was characterized with significantly larger size, connective tissue content, and significantly lower cellularity, in relation to the first type. Such glomeruli might be considered as hypertrophic. First type of glomeruli was predominant in younger cases, while second type of glomeruli was predominant in cases older than 55 years.

The newly developed mononuclear 5,6-epoxy-5,6-dihydro-1,10phenanthroline platinum(II) complex revealed notable antitumor effects in vitro and in vivo. In this study, the effects of this platinum(II) complex on the immune response were assessed. Peritoneal macrophages and splenocytes obtained from mice were treated with lipopolysaccharide (LPS)/Concanavalin A (ConA) along with platinum(II) complex and measurement of cytokine concentrations and immunophenotyping was performed. Our findings indicate that the platinum(II) complex exhibits significant immunomodulatory effects on peritoneal macrophages and splenocytes.

The immune checkpoint axis PD-1/PD-L1 is a cornerstone of cancer immunotherapy. However, its efficacy in breast cancer is often limited by a complex and immunosuppressive tumour microenvironment (TME). The IL-33/ST2 signalling pathway, a key player in type 2 inflammation, is increasingly recognized for its pro-tumoral roles in various cancers, contributing to immune evasion and metastasis. This review explores the synergistic potential of combining PD-1/PD-L1 blockade with IL-33/ST2 inhibition to overcome therapeutic resistance and enhance anti-tumour immunity in breast cancer. Current literature on the PD-1/PD-L1 and IL-33/ST2 pathways in breast cancer progression was synthesized, focusing on their mechanisms of immune suppression and TME modulation. It examines preclinical and clinical data on the individual and combined therapeutic strategies targeting these pathways. Evidence suggests that IL-33 signalling promotes a suppressive TME by recruiting regulatory T cells, myeloid-derived suppressor cells, and M2 macrophages, which can limit the effectiveness of PD-1/PD-L1 inhibitors. Conversely, blocking the IL-33/ST2 pathway has been shown to reprogram the TME, leading to increased infiltration of cytotoxic T lymphocytes and enhanced anti-tumour responses. Therefore, a dual-targeting approach is proposed to simultaneously disarm these two distinct but cooperative immune evasion mechanisms. Dual blockade of PD-1/PD-L1 and IL-33/ST2 signalling pathways represents a novel and promising strategy to enhance the efficacy of immunotherapy in breast cancer. This approach has the potential to revert the immunosuppressive TME, leading to more durable and robust anti-tumour responses. Further research is warranted to validate this hypothesis and translate it into effective clinical trials.

Introduction: Immune checkpoint therapy is well- established therapeutic approach in treatment of malignant disease and is thought to be mostly based on facilitating adaptive immune responses. However, cells of innate immune response, such as NKT cells, might also be important for successful anti-programmed cell death protein 1 therapy, as they initiate anti-tumor immune response. Materials and methods: For tumor induction, 4T1 cells syngenic to BALB/c background were used after which mice underwent anti-programmed cell death protein 1 treatment.After the mice were sacrificed, NKT cells, dendritic cells and macrophages derived from spleen and primary tumor tissue were analyzed using flow cytometry. Results: Anti-programmed cell death protein 1 therapy significantly decelerates tumor growth and enhanced expression of activating molecules CD69, NKp46, NKG2D in NKT cells of tumor and spleen. Anti-programmed cell death protein 1 therapy activates pro-tumoricidic changes in dendritic cells and macrophages of primary tumor tissue. Conclusion: Anti-programmed cell death protein 1 therapy activates NKT cell directly, and indirectly via DCs. Activated NKT cells provide tumoricidic properties directly, by secreting perforin, and indirectly by stimulating M1 macrophages polarization. Since anti-programmed cell death protein 1 therapy induces significant changes in NKT cells, dendritic cells and macrophages, efficacy of overall anti-programmed cell death protein 1 therapy is increased, contributing to more efficient anti-tumor immune response.