Aim: To enhance the effectiveness and safety of sun protection product use by developing recommendations based on an analysis of the Ukrainian SPF product market.

Materials and Methods: A literature review was conducted using publications indexed in the databases Google Scholar, Web of Science, and Scopus, and the PubMed and ToxNet search engines. A structured search was conducted using relevant keywords and their logical combinations, including: "skin cancer" and "ultraviolet radiation", "sunscreens", "SPF products", "sunscreen cosmetics", "efficacy and safety of sunscreens", and others. Information about sunscreens contained only on the official websites of the manufacturers was used. Information from unofficial sources was not considered. The review is based mainly on recent studies; however, selected scientific sources (2011-2018) were intentionally included to highlight the evolution of scientific knowledge in this field. The analysis used formal-logical and systemic-complex methods, which ensured a comprehensive and critical synthesis of the available evidence.

Conclusions: Ultraviolet radiation is the main factor in the development of melanoma, basal cell carcinoma, and squamous cell carcinoma of the skin. The increasing incidence of skin cancer prompts health professionals to encourage the population to use sunscreens. Sun protection factor (SPF) serves as the main criterion for choosing the necessary level of protection in conditions of insolation. International recommendations support the use of preparations with high SPF indices, but in practice, frequent cases of inaccurate information provided by cosmetic manufacturers have been recorded. At the same time, cosmetic sunscreens, even with the same SPF value, demonstrate different levels of effectiveness under insolation conditions. The Ukrainian cosmetic market offers hundreds of SPF products in the form of creams, sprays, oils, milks, or foams. In addition to well-known brands from France, the USA, Italy, Switzerland, Germany, Poland, and Ukraine, dozens of brands from lesser-known manufacturers, especially from Korea, are now available thanks to online shopping. As a rule, such resources do not indicate the exact SPF used in the product but instead declare marketing characteristics such as "lightest" or "safest." Today, their use is gaining popularity among the population; however, the need for legislative control over them must be addressed.

Delayed chemotherapy-induced nausea and vomiting (CINV) in pediatric oncology patients is currently under-recognized. This study aims to develop, validate, and visualize a machine learning-based model to predict delayed CINV risk in children.

This prospective cohort study was conducted from November 2021 to December 2022 at a tertiary hospital in southern China. Pediatric delayed CINV data were collected via an electronic diary using the Pediatric Nausea Assessment Tool (PeNAT) and National Cancer Institute-Common Terminology Criteria for Adverse Events (NCI-CTCAE) (v4.03), with PeNAT ≥3 or CTCAE grade ≥2 as the primary outcomes. Seven machine learning models, including random forest, support vector machine, and artificial neural network (ANN), were developed and validated using 29 sociodemographic and clinical features. Model performance was assessed using the area under the receiver operating characteristic curve (AUC) and other metrics. Shapley's Additive Explanations (SHAP) enhanced interpretability, and the models were integrated into a web-based calculator for visualization.

Overall, 399 pediatric patients (60.4% male; aged 4-18 years) were included. The AUC of the seven models ranged from 0.782 to 0.815, with the ANN model performing best (AUC 0.815; 95% CI, 0.695-0.903). The ANN model's global SHAP plot revealed that the most influential features were acute CINV, days of chemotherapy, age, number of recreational activities, expectancy of CINV, and control effectiveness of CINV. The ANN model was then deployed as a web-based risk calculator for pediatric delayed CINV.

The ANN model demonstrated good performance in identifying children at high risk of delayed CINV. Our web-based calculator provides a reliable tool for clinical staff to support targeted CINV management.

Extracellular matrix (ECM) detachment is crucial for metastasis in cancer cells. During tumorigenesis, a programmed cell death occurs to clear off the ECM detached cancer cells in the circulatory system; this phenomenon is referred to as anoikis. Metastatic cancer cells can evade anoikis by regulating mechanisms such as cell adhesion, cell growth, oxidative stress, cancer stemness, hypoxia and metabolic reprogramming. Studies have shown that RNA modifications regulate multiple cancer mechanisms; however, the role of RNA modifications in anoikis resistant is not established yet. Therefore, in this study, we assessed the role of N6-methyladenosine (m6A) modification of mRNAs in anoikis resistant conditions. First, we cultured cancer cells in low adhesive plates for six (6) days followed by quantitative real-time PCR (qRT-PCR) of major m6A regulators and quantification of the global m6A levels in detached versus attached cancer cells. We also assessed cell proliferation in detached cancer cells using STM2457, a potent and specific METTL3 inhibitor. Our results showed a significant (p < 0.05) increase in METTL3 expression and activity in anoikis resistant cancer cells. Furthermore, we observed an elevation in global m6A levels on mRNAs. Treatment of anoikis resistant cancer cells with STM2457 caused reduction in spheroid size, induction of apoptosis, and cell cycle arrest which were correlated with a decrease in global m6A levels. Conclusively, our findings reveal that METTL3-dependent m6A methylation sustains the survival and proliferation of anoikis-resistant cancer cells, highlighting an epitranscriptomic mechanism underlying metastatic fitness.

Triple-negative breast cancer (TNBC) is a clinically aggressive subtype with limited therapeutic strategies. Although long non-coding RNAs (lncRNAs) are increasingly linked to tumor progression, their regulatory role in macrophage polarization during TNBC remains unclear. This study investigates the molecular interplay between lncRNA PVT1 and PPARγ in driving macrophage reprogramming during TNBC progression. Utilizing an orthotopic TNBC mouse model, single-cell RNA sequencing (scRNA-seq) identified nine distinct cell types, with pseudotime trajectory analysis revealing macrophage accumulation in advanced tumor stages. Reannotation of macrophages highlighted M2-like polarization dominance during TNBC development. Bulk sequencing of TNBC macrophages and integrated GEO/TCGA analyses identified PPARγ as a key regulator and PVT1 as a differentially expressed lncRNA in TNBC versus normal tissues. In vitro experiments with THP-1/U937 macrophages demonstrated that PVT1 knockdown or PPARγ modulation altered macrophage polarization, subsequently affecting MDA-MB-231 and MCF-7 breast cancer cell proliferation and invasion. Mechanistically, RNA/DNA pulldown and luciferase assays confirmed that PVT1 recruits NOP56 and E2F1 to form a transcriptional complex, enhancing E2F1-driven PPARγ expression. In vivo, orthotopic tumors generated from PVT1-silenced THP-1/MDA-MB-231 cell mixtures exhibited suppressed growth, increased M1-like macrophages, and elevated apoptosis (TUNEL assay), whereas PPARγ overexpression accelerated tumor progression with M2-dominant infiltration (flow cytometry). These findings establish lncRNA PVT1 as a critical epigenetic scaffold coordinating NOP56-E2F1-PPARγ signaling to polarize macrophages toward a pro-tumorigenic M2 phenotype, thereby fueling TNBC aggressiveness. This study unveils novel therapeutic targets for TNBC by disrupting the PVT1-PPARγ axis to rebalance macrophage dynamics and induce tumor-suppressive immunity.

The hypoxic, nutrient-deprived tumour microenvironment (TME), a hallmark of solid tumours, imposes cellular stress that can also paradoxically promote survival and resistance. While TP53 is the most frequently mutated gene in cancer, approximately 60% of hepatocellular carcinoma (HCC) cases retain wild-type TP53 (WTp53), suggesting its isoforms as potential tumorigenic modulators that override canonical tumour-suppressive functions. Therefore, this study aims to delineate p53 isoform profiles in response to short-term hypoxia and nutrient deprivation, recapitulating key stressors in the tumour biology.

We hereby established a 7-day HepG2 tumoursphere model by seeding 15,000 cells/well, which transitioned from normoxia (4 days) to a hypoxic (1% O₂), low-serum (1% FBS) (HLS) condition (3 days). Expression of p53 isoforms and downstream targets was assessed.

The formation of HepG2 tumoursphere at different seeding densities determined the diameter, viability and proliferation profiles, with 15,000 cells/well producing optimal, viable tumourspheres with the highest yield. HLS conditions significantly reduced tumoursphere size, proliferation capacity and viability. Strikingly, multiplex long-amplicon ddPCR revealed substantial upregulation of FLp53α/Δ40p53α, Δ40p53α and Δ133p53α/Δ160p53α mRNA transcripts. While FLp53α/Δ40p53α remained dominant, Δ40p53α and Δ133p53α/Δ160p53α progressively increased, altering the balance among the isoforms. This shift correlated with enhanced expression of the pro-proliferative and survival markers (PCNA and BCL2) and reduced expression of the pro-apoptotic marker (BAX) and cell cycle inhibitor (CDKN1A), suggesting a potential functional role of these isoforms in promoting tumour cell adaptation under stress.

This study highlights stress-induced p53 isoform modulation as a potential survival mechanism in WTp53 HCC in response to TME stress, which warrants further exploration of isoform-specific p53 functions in understanding heterogeneity, resistance and cancer recurrence.

Copper is essential for cellular homeostasis and can induce cuproptosis, a novel form of cell death. However, its effect on cancer progression, specifically through the regulation of epithelial-mesenchymal transition (EMT)-a primary driver of metastasis and treatment resistance in human cancers-remains unclear. This study assessed the dual role of copper in colorectal cancer cells, focusing on the polo-like kinase 1-forkhead box O3a-beta catenin (PLK1-FOXO3a-β-catenin) signaling pathway. Treatment with CuCl₂ (hereby referred to as Cu) alone facilitated EMT in SW480 and LoVo cells by upregulating PLK1 and downregulating FOXO3a that enhanced β-catenin activity without inducing cell death. In contrast, co-treatment with Cu and copper ionophore elesclomol (Cu-ES) triggered cuproptosis, a unique copper-dependent form of cell death, accompanied by mitochondrial dysfunction, dihydrolipoamide S-acetyltransferase aggregation, and ATP depletion. Specifically, Cu-ES treatment suppressed EMT by reducing PLK1 and activating FOXO3a that suppressed β-catenin-mediated transcription. Additionally, while Cu treatment alone had minimal effect on FOXO3a nuclear localization, Cu-ES treatment significantly enhanced FOXO3a nuclear translocation and its interaction with β-catenin, resulting in EMT gene repression. The PLK1 inhibitor BI-2536 recapitulated the effects of Cu-ES and exhibited synergistic activity when combined with Cu-ES, enhancing both cell death and EMT suppression. These findings highlight a novel regulatory mechanism of EMT through copper signaling and support copper-based combination therapies as a promising approach to simultaneously inhibit tumor growth and metastasis in colorectal cancer.

Circular RNAs (circRNAs) have been identified as important mediators of tumorigenesis and tumor progression. This study focuses on circAGFG1, a circRNA with elevated N6-methyladenosine (m6A) modification, and its role in triple-negative breast cancer (TNBC). Fluorescence in situ hybridization and qPCR analyses revealed that circAGFG1 is significantly upregulated in TNBC tissues and in the TNBC cell line MDA-MB-231. Functional characterization using loss-of-function and gain-of-function strategies in two TNBC cell lines demonstrated that circAGFG1 promotes oncogenic phenotypes. Specifically, knockdown in MDA-MB-231 cells suppressed proliferation, invasion, migration, and G1/S phase transition, while its overexpression in MDA-MB-468 cells promoted these processes. Mechanistically, western blotting and PCR analyses indicated that circAGFG1 modulates the expression of epithelial-mesenchymal transition markers N-cadherin and α-SMA. Furthermore, we identified that YTHDF3, an m6A reader protein upregulated in TNBC, upregulates circAGFG1 expression by enhancing its transcript stability. Finally, dual-luciferase reporter assays confirmed that circAGFG1 acts as a sponge for miR-1299, thereby potentially modulating the miR-1299 signaling pathway. Collectively, our findings delineate the critical role of the circAGFG1 in promoting TNBC progression, highlighting its potential as a novel therapeutic target.

Aim: This study aimed to evaluate the incidence of postpancreatoduodenectomy acute pancreatitis (PPAP) and analyze its association with histological and oncological features of the resected tumors.

Materials and Methods: Data from 296 patients who underwent PD between 2014 and 2023 were analyzed. The intergroup analysis compared patients in the PPAP (n=126) and no-PPAP (n=170) groups regarding tumor histology, stage, differentiation, resection margin status, and type of PD.

Results: PPAP occurred in 42,6% of cases, and clinically relevant PPAP in 30,1%. PPAP was more common in patients with cystic pancreas neoplasms (22,4% in the PPAP group vs. 9,0% in the no-PPAP group, p=0,001) and duodenal adenocarcinoma (4,0% vs. 0,6%, p=0,04) and tended to occur more often in distal bile duct adenocarcinoma (10.4% vs. 4.8%, p=0.07). In contrast, patients with pancreatic ductal adenocarcinoma had a lower PPAP rate (22,4% vs. 49,1%, p<0,0001). The tumor size (T1-T4) and differentiation (G1-G4) did not affect PPAP incidence. A higher incidence of PPAP was observed in the N0 group (46,7% vs. 30,8%, p=0,03), as well as in patients with R0 resections (91,0% vs. 70,3%, p=0,0006). Standard PD was also associated with a higher frequency of this complication (the difference at borderline significance: p=0,05).

Conclusions: The incidence of PPAP is associated with certain histological tumor types and the extent of surgery. Tumor size and grade of differentiation had no significant impact, while N0 lymph node status and R0 resection margins were associated with higher PPAP incidence.

Aim: To assess the potential impact of mine water contamination on the increased risk of malignant neoplasms among the population of an industrially affected region of Ukraine (Kryvyi Rih Iron Ore Basin).

Materials and Methods: Hygienic, epidemiological and statistical methods of research were used in the study. The study of mine water was conducted using samples obtained from 63 points representing the main mining horizons of the Kryvyi Rih Iron Ore Basin (Ukraine), using the following indicators: dissolved oxygen, biochemical oxygen demand over 5 days (BOD₅), hydrogen index (pH), suspended solids, chemical oxygen demand (COD), dry residue, chlorides, sulfates, ammonium nitrogen, nitrites, nitrates, phosphates, oil products, total iron, and phenols.

Results: Laboratory analysis of mine water revealed that the concentrations of several substances exceeded permissible levels. The integral pollution coefficients suggested the water to be extremely polluted, and the ecological state of the environment as critical. The risk of malignant neoplasms in the Kryvyi Rih industrial region was 25,054 (95% CI 25,010-25,098). Teenagers aged 15-17 had the highest risk of developing malignant neoplasms (OR 16,310 [95% CI 5,927-44,888]). Children under the age of 14 ranked second (OR 5,528 [95% CI 3,423-8,925]). Adults (≥18 years old) had a lower risk of malignant neoplasms (OR 2,461 [95% CI 2,309-2,622]). Children and adolescents were more affected than adults, i.e. the etiologic fraction of mine water pollution in the development of malignant neoplasms was 81,9% and 94,3%, respectively (vs. 59,6% in adults).

Conclusions: Considering the extremely polluted state of mine waters in the industrially affected region of Ukraine, and assessing the related malignant neoplasm risks in the context of public health, the development of innovative preventive strategies and methodologies is required, taking into account all relevant determinants, including environmental factors.

Direct oral intervention of spleen aminopeptide (SA) would be limited because of its varied swelling and release rate in different pH environments of digestive fluids. Herein, pH-responsive hydrogel microspheres (3.67 ± 0.04 mm) with positive SA-loaded chitosan (Cs) core and negative alginate (ALG) shell were prepared. Entrapment efficiency was 76.22% and loading rate of SA was 35.17%. Besides the hydrogen bonding, a strong core/shell structure was constructed by forming imine bond via the Schiff base reaction of amino group in Cs with ketone group on SA. In vitro simulated digestion showed that the swelling rate of microspheres was 192.8% (pH 1.2), 2481.5% (pH 6.8), and 1144.3% (pH 7.4). The release rate of SA was 0.9% in simulated gastric fluid for 2 h, 6.0% in simulated intestinal fluid for 2 h and continuous release in simulated colonic fluid for 24 h with a cumulative release rate of 92.4%. After treatment, the observation group exhibited increasing levels of CD3⁺, CD4⁺, CD4⁺/CD8⁺, IgA, IgG and IgM. Total effective rate in observation group was 96.15%, being higher than that in control group (84.31%). This work provided a valuable reference for preparing drug-loaded hydrogels to improve the recurrent respiratory infection in children.