This study aimed to assess the expression profile of messenger RNA (mRNA) and microRNA (miRNA) related to the dopaminergic system in five types of breast cancer in Polish women. Patients with five breast cancer subtypes were included in the study: luminal A (n = 130), luminal B (n = 196, including HER2−, n = 100; HER2+, n = 96), HER2+ (n = 36), and TNBC (n = 43); they underwent surgery, during which tumor tissue was removed along with a margin of healthy tissue (control material). The molecular analysis included a microarray profile of mRNAs and miRNAs associated with the dopaminergic system, a real-time polymerase chain reaction preceded by reverse transcription for selected genes, and determinations of their concentration using enzyme-linked immunosorbent assay (ELISA). The conducted statistical analysis showed that five mRNAs statistically significantly differentiated breast cancer sections regardless of subtype compared to control samples; these were dopamine receptor 2 (DRD2), dopamine receptor 3 (DRD3), dopamine receptor 25 (DRD5), transforming growth factor beta 2 (TGF-β-2), and caveolin 2 (CAV2). The predicted analysis showed that hsa-miR-141-3p can regulate the expression of DRD2 and TGF-β-2, whereas hsa-miR-4441 is potentially engaged in the expression regulation of DRD3 and DRD5. In addition, the expression pattern of DRD5 mRNA can also be regulated by has-miR-16-5p. The overexpression of DRD2 and DRD3, with concomitant silencing of DRD5 expression, confirms the presence of dopaminergic abnormalities in breast cancer patients. Moreover, these abnormalities may be the result of miR-141-3P, miR-16-5p, and miR-4441 activity, regulating proliferation or metastasis.

The aim of this study was to identify miRNAs that could potentially influence the activity of SMAD proteins involved in TGFβ signal transduction in five types of breast cancer in Polish women. Patients with five breast cancer subtypes were included in the study: luminal A (n = 130), luminal B HER2− (n = 100), luminal B HER2+ (n = 96), non-luminal HER2+ (n = 36), and TNBC (n = 43). During surgery, tumor tissue was removed along with a margin of healthy tissue (control). Molecular analysis included determination of the expression of genes related to SMAD protein signal transduction using mRNA microarrays and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Protein expression was determined using an enzyme-linked immunosorbent assay (ELISA). The miRNA profiling was performed using miRNA microarrays and the miRDB database. SMAD3 and SMAD5 were overexpressed in all types of breast cancer, which could be related to the reduced expression of miR-145, and the findings for SMAD4 and miR-155 were similar. Additionally, the level of SMAD7 was reduced, which may be due to the low activity of miR-15b and miR21b. This study determined the gene expression profiles involved in SMAD protein signal transduction across five different types of breast cancer and identified the miRNAs potentially regulating their activity. Overexpression of SMAD3, SMAD4, and SMAD5 suggests excessive activation of the TGFβ pathway, potentially promoting tumor growth and development. Concurrently, a significant reduction in SMAD7 expression removes inhibitory control in the TGFβ pathway, a phenomenon that is particularly evident in more aggressive breast cancer types.

Background/Objectives: In this study, serum selenium levels in patients with Crohn’s disease (CD) and ulcerative colitis (UC) were evaluated to identify potential predictive markers of disease activity. Conducted in 100 inflammatory bowel disease (IBD) patients (54 CD, 46 UC) and 100 healthy controls, this research provides novel insights through focusing on the regional selenium status of people with IBD in the Polish population, a demographic with limited existing data. Methods: Selenium concentrations were measured using inductively coupled plasma mass spectrometry (ICP-MS). Results: Significantly lower levels of selenium were observed in CD (64.79 µg/L ± 12.15 µg/L) and UC (68.61 µg/L ± 11.43 µg/L) patients when compared with the controls (90.52 ± 12.00 µg/L, p < 0.0001). Regression analysis identified leukocyte and erythrocyte counts and bilirubin as significant predictors of selenium levels in UC patients, while no significant predictors were found for CD. Conclusions: The findings suggest that selenium deficiency is linked to IBD and may serve as a non-invasive biomarker for disease severity, particularly in UC. This practical approach offers a potential alternative to invasive procedures such as endoscopy for monitoring disease progression. However, further research is needed to confirm these findings in larger populations and explore the therapeutic role of selenium supplementation in IBD management.

Background/Objectives: Endometrial cancer (EC) is a multifactorial disease influenced by metabolic, hormonal, and environmental factors. Trace and macroelements play a critical role in cellular homeostasis, oxidative stress, and tumor progression; however, their relationship with EC grading and clinical characteristics remains insufficiently understood. Methods: This study evaluated the concentrations of selected macro- and trace elements (Na, K, Ca, P, Mg, Mn, Cu, Zn, Be, As, Cr, Mo, Ti, Tl, Pb) in patients with endometrial cancer (G1–G3) and a control group (C). Elemental analysis was performed using inductively coupled plasma optical emission spectrometry (ICP-OES). Associations between elemental concentrations and clinicopathological variables, including age, body mass index (BMI), menopausal status, diabetes, and smoking, were assessed using appropriate statistical tests, including ANOVA with Tukey’s post hoc analysis and Student’s t-test. Multivariate regression analysis was performed to identify independent predictors of elemental alterations. Results: Significant differences in elemental concentrations were observed across EC grading. Higher-grade tumors were associated with increased levels of Ca, P, Mg, and Mn, while Na and K showed a decreasing trend with tumor progression. No statistically significant differences were observed for Zn, Ti, Tl, or Pb across histological grades. Stratified analyses demonstrated that clinical and metabolic factors had a limited and selective impact on elemental profiles. Age and BMI were associated with minor variations in selected elements, whereas menopausal status, diabetes, and smoking showed predominantly non-significant or inconsistent effects. Multivariate analysis identified histological grade as the primary determinant of elemental alterations, while other variables exhibited weaker or element-specific associations. Conclusions: Elemental homeostasis in endometrial cancer is primarily associated with tumor progression rather than systemic metabolic or lifestyle factors. Changes in Ca-, P-, Mg-, and Mn-related pathways may reflect tumor-driven metabolic reprogramming, whereas most trace elements remain relatively stable. These findings suggest that elemental profiling may provide insight into EC biology, although its clinical utility requires further investigation.

Breast cancer (BC) comprises heterogeneous subtypes with distinct molecular drivers and clinical behaviors. Among the key signaling pathways implicated in BC progression is the mitogen-activated protein kinase (MAPK) cascade, which regulates cell proliferation, apoptosis, and stress responses. microRNAs (miRNAs), as post-transcriptional regulators, are increasingly recognized as modulators of MAPK-associated genes, yet their integrated role across BC subtypes remains incompletely understood. This study included 405 patients with histopathologically confirmed BC, stratified into luminal A (LumA), HER2-negative luminal B, HER2-positive luminal B, non-luminal HER2-positive, and triple-negative breast cancer (TNBC). Control tissues were obtained from matched surgical margins. We performed mRNA profiling (Affymetrix microarrays), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), protein quantification (enzyme-linked immunosorbent assay (ELISA), and miRNA expression analysis. Predicted miRNA-mRNA interactions were analyzed using the miRDB database. Functional protein–protein interactions were explored using the STRING database. MAP3K1, MAP2K4, and TP53 were significantly downregulated across all subtypes, while PPM1D, LMTK3, and TGFB1 were upregulated, especially in TNBC. These alterations were supported by concordant changes at the protein level. Dysregulated miRNAs—miR-21-3p, miR-23c, miR-27a-3p, miR-205-3p, and miR-300—exhibited in-verse expression patterns relative to their predicted target genes. STRING analysis identified TP53 as a central hub, linking MAPK signaling with stress and apoptotic pathways. This integrated transcriptomic and miRNA profiling study reveals subtype-specific dysregulation of MAPK-associated genes and their miRNA regulators in BC, with TNBC exhibiting the most profound alterations. These findings provide insight into potential targets for personalized therapeutic strategies.

Introduction: Interactions between extracellular signals with the extracellular matrix (ECM) influence cellular phenotype and molecular functions, affecting proliferation, differentiation, adhesion, apoptosis, and migration. Deregulation of ECM remodeling contributes to the development of diseases, including breast cancer. The study aimed was to identify microRNAs (miRNAs) that may regulate the activity of genes involved in ECM remodeling and focal adhesion across five breast cancer subtypes in Polish women.Material and methods: The study enrolled patients representing five breast cancer subtypes: 130 luminal A, 100 HER2-negative luminal B, 96 HER2-positive luminal B, 36 non-luminal HER2-positive, 43 triple-negative breast cancer (TNBC) cases. Cancer tissue samples were collected during surgery along with adjacent healthy tissue margins (control group). The expression profiles of genes associated with ECM remodeling and focal adhesion were evaluated with mRNA microarrays and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Protein expression was assessed using enzyme-linked immunosorbent assay (ELISA). miRNA detection and target prediction were performed using miRNA microarrays.Results: Overexpression of COL1A1, FN1, ITGB1, and THBS1 may be associated with reduced levels of miR-129, miR-432, miR-124, miR-384, respectively. Decreased COL6A6 expression may result from increased activity of miR-1246. Additionally, the study revealed increased levels of COL1A2, COMP, SPP1 with reduced activity of RELN, across all five breast cancer subtypes.Conclusions: This is the first study to comprehensively analyze miRNA-mediated regulation of ECM-related genes across five breast cancer subtypes in a Polish cohort. Overexpression of COL1A1, FN1, and ITGB1 is linked to reduced levels of specific miRNAs, while decreased COL6A6 expression is associated with increased miR-1246 activity.