Semaglutide, a glucagon-like peptide 1 receptor agonist, is an antidiabetic that has recently shown promising immunomodulatory and antitumor effects. Breast cancer is the most common type of cancer affecting women worldwide. The aim of this study was to analyze the effects of semaglutide on the antitumor immunity in a 4T1 mouse breast cancer model. After induction of breast cancer, BALB/C mice were treated intraperitoneally with semaglutide. Semaglutide administration decelerated tumor appearance, growth and progression. The antidiabetic drug showed neither a direct cytotoxic effect in vitro, nor an angiogenic effect. Furthermore, depletion of NK cells had no affect on tumor growth in semaglutide treated mice suggesting a non-NK cell-dependent mechanism. However, semaglutide increased the accumulation and maturation of CD11c⁺ dendritic cell, while decreasing the percentage of FoxP3⁺ regulatory T cells in the spleen and primary tumor. In addition, semaglutide increased tumor infiltration and promoted the antitumor phenotype of T cells, in vivo. Furthermore, semaglutide enhanced the cytotoxic capacity of CD8⁺ T cells, in vitro. These results suggest that semaglutide enhances the acquired antitumor immune response and has potential for the future treatment of malignancies.

The essential oil derived from the bark of Cinnamomum zeylanicum L., Lauraceae, has gained significant attention because of its numerous biological benefits. This study aimed to perform a phytochemical analysis of commercially available Cinnamomum zeylanicum bark essential oil and to evaluate its antioxidant, antimicrobial, immunomodulatory, and antitumor properties. GC–MS analysis was employed to determine the phytochemical composition. The major component of the total essential oil composition was (E)-cinnamaldehyde, constituting 77.93%, followed by eugenol (4.34%), E-caryophyllene (3.68%), and linalool (2.79%). The antioxidant activity was confirmed by DPPH, ABTS, CUPRAC, and TAC assays. In the broth microdilution assay, cinnamon essential oil demonstrated strong antimicrobial activity, with MIC values ranging from 7.37 to 29.50 µg/mL. Furthermore, cinnamon essential oil demonstrated selective antitumor activity by inducing apoptosis and cell-cycle arrest in human colorectal cancer cells (HCT116) while sparing non-cancerous cells (MRC-5). In HCT116 cells, cinnamon essential oil induced apoptosis, downregulated Cyclin D and p-AKT, and caused G1-phase arrest. Additionally, cinnamon essential oil modulated immune responses by reducing pro-inflammatory cytokine production in activated splenocytes and enhancing pro-inflammatory activity in naïve cells. These findings highlight the great potential of the cinnamon bark essential oil in the development of new therapeutic agents.

Heyde syndrome, marked by aortic stenosis, gastrointestinal bleeding from angiodysplasia, and acquired von Willebrand syndrome, is often underreported. Shear stress from a narrowed aortic valve degrades von Willebrand factor multimers, leading to angiodysplasia formation and von Willebrand factor deficiency. This case report aims to raise clinician awareness of Heyde syndrome, its complexity, and the need for a multidisciplinary approach. We present a 75-year-old man with aortic stenosis, gastrointestinal bleeding from angiodysplasia, and acquired von Willebrand syndrome type 2A. The patient was successfully treated with argon plasma coagulation and blood transfusions. He declined further treatment for aortic stenosis but was in good overall health with improved laboratory results during follow-up. Additionally, we provide a comprehensive review of the molecular mechanisms involved in the development of this syndrome, discuss current diagnostic and treatment approaches, and offer future perspectives for further research on this topic.

A series of mono- and heteronuclear platinum(II) and zinc(II) complexes with 4,4′,4″-tri-tert-butyl-2,2′:6′,2″-terpyridine ligand were synthesized and characterized. The DNA and protein binding properties of [ZnCl₂(terpy^tBu)] (C1), [{cis-PtCl(NH₃)₂(μ-pyrazine)ZnCl(terpy^tBu)}](ClO₄)₂ (C2), [{trans-PtCl(NH₃)₂(μ-pyrazine)ZnCl(terpy^tBu)}](ClO₄)₂ (C3), [{cis-PtCl(NH₃)₂(μ-4,4′-bipyridyl)ZnCl(terpy^tBu)}](CIO₄)₂ (C4) and [{trans-PtCl(NH₃)₂(μ-4,4′-bipyridyl)ZnCl(terpy^tBu)}](CIO₄)₂ (C5) (where terpy^tBu = 4,4′,4″-tri-tert-butyl-2,2′:6′,2″-terpyridine), were investigated by electronic absorption, fluorescence spectroscopic, and molecular docking methods. Complexes featuring transplatin exhibited lower K_b and K_sv constant values compared to cisplatin analogs. The lowest K_sv value belonged to complex C1, while C4 exhibited the highest. Molecular docking studies reveal that the binding of complex C1 to DNA is due to van der Waals forces, while that of C2–C5 is due to conventional hydrogen bonds and van der Waals forces. The tested complexes exhibited variable cytotoxicity toward mouse colorectal carcinoma (CT26), human colorectal carcinoma (HCT116 and SW480), and non-cancerous mouse mesenchymal stem cells (mMSC). Particularly, the mononuclear C1 complex showed pronounced selectivity toward cancer cells over non-cancerous mMSC. The C1 complex notably induced apoptosis in CT26 cells, effectively arrested the cell cycle in the G0/G1 phase, and selectively down-regulated Cyclin D.

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.