Hepatocellular carcinoma is one of the most aggressive malignancies worldwide, with limited therapeutic options. Boswellia serrata Roxb., an Indian medicinal tree, produces a resin rich in essential oil and boswellic acids, particularly acetyl-11-keto-β-boswellic acid (AKBA), with demonstrated antiproliferative and pro-apoptotic activities. This study investigated the cytotoxic effects of B. serrata essential oil and AKBA on hepatocarcinoma Huh-7 cells in both monolayer and three-dimensional spheroid cultures and characterized the underlying molecular targets. Essential oil was extracted and analyzed by gas chromatography-mass spectrometry (GC-MS). Cytotoxicity was assessed using the cell counting kit-8 (CCK-8). Three-dimensional spheroid cultures were also established to evaluate anti-tumoral potential. Expression of cyclin D1, cyclin-dependent of kinase 4 (CDK4) (cyclin-dependent kinase inhibitor 1A (p21), E-cadherin, (alpha fetoprotein) AFP, epithelial cell adhesion molecule (EpCAM), Myeloid cell leukemia-1 (Mcl-1), and caspase-3 was analyzed by western blot. In addition, an in silico analysis was performed on the main constituents of B. serrata essential oil targeting 5-lipoxygenase (5LO). The results showed cytotoxic effects, with AKBA exhibiting greater potency than the essential oil. Cytotoxicity was associated with caspase-3-mediated apoptosis, with minimal effects on cell cycle and epithelial-mesenchymal transition markers. The in silico analysis predicted that some compounds may act as competitive inhibitors of the 5LO at the catalytic site and partially activate pro-apoptotic pathways. These data support the potential of B. serrata-derived compounds as novel anti-hepatocarcinoma agents, with AKBA and longifolene as leads for further preclinical and clinical research.

Prostate cancer (PCa) is one of the most common causes of cancer-related mortality in men globally. Although current therapies can control early-stage disease, advanced PCa remains difficult to treat because of therapeutic resistance and adverse side effects, highlighting the need for new treatment strategies. Syzygium nervosum (SN), a medicinal plant rich in bioactive compounds such as gallic acid and ellagic acid, has demonstrated anticancer properties in several malignancies; however, its effects on PCa remain unclear. This study investigated the anticancer potential of SN using integrated computational and in vitro approaches. DU145 and PC-3 prostate cancer cells were treated with SN extract at concentrations of 25-400 µg/mL for 24 and 48 h. Cell viability, colony formation, and cell-cycle progression were evaluated to determine antiproliferative activity. In parallel, computational analyses were performed to predict molecular targets of SN-derived compounds. Our results displayed that SN extract reduced cell viability, suppressed clonogenic growth, and disrupted cell-cycle progression in both cell lines. Computational findings suggested that gallic and ellagic acids may interact with key regulatory proteins related to cell proliferation and survival, including AKT and CDK2. Overall, SN demonstrates promising anticancer activity and may represent a potential therapeutic source for prostate cancer treatment.

Non-Hodgkin lymphomas (NHL) are lymphoproliferative neoplasms with a heterogenous genetic landscape that require multiple assays to be characterized. Cytological samples are frequently utilized in the diagnosis of NHL. An RNA-based assay was utilized to detect translocations and identify mutations in fine-needle aspiration cytology (FNAC) samples of NHL. Fragmentation index and RNA concentration were evaluated in 54 FNAC and eight corresponding histological samples of NHL to establish first the material adequacy before sequencing. To sequence FusionPlex Lymphoma (ArcherDX, Boulder, USA), an anchored multiplex polymerase chain reaction-based RNA targeting 125 genes was used. The sequencing data processing was entirely carried out on the ArcherDX online platform. Mutations were detected in 21 of 62 samples (34%), and in 41 of 62 samples (66%), no genomic alterations were found. The FusionPlex assay detected five BCL6 translocations (three IGH-BCL6 and two EIF4A2-BCL6), six IGH-BCL2 translocations, two IGH-CCND1 translocations, two TP53 point mutations, two MYD88 mutation and four uncommon translocations (two EIF4E3-FOXP1, one TBL1XR1-TP63, one LOC105370537-FUT8). In eight out of eight cases, there was NGS (Next Generation Sequencing) results concordance between corresponding cytological and histological samples (100% concordance). FNAC samples of NHL are suitable for molecular assessment by NGS and FusionPlex Lymphoma assay is an effective method for this purpose. NGS allows the detection of mutations and the identification of translocations on cytological samples also with scanty diagnostic material.

Prostate cancer remains one of the most biologically heterogeneous malignancies in men and continues to present major therapeutic challenges despite advances in androgen receptor-targeted therapy and molecular stratification. Increasing evidence suggests that prostate cancer progression is influenced not only by tumor-intrinsic genetic alterations but also by complex interactions involving androgen receptor signaling, inflammatory pathways, metabolic reprogramming, oxidative stress, epigenetic remodeling, immune dysregulation, and gut microbiome-associated signaling. Within this evolving systems-level framework, natural products have attracted increasing attention because of their ability to modulate multiple interconnected molecular pathways. This review examines the molecular basis of prostate cancer progression with particular emphasis on crosstalk among androgen receptor signaling, microbiome-associated regulation, epigenetic adaptation, inflammatory signaling, and tumor microenvironment remodeling. The emerging role of the gut microbiome in androgen metabolism, microbial metabolite production, immune regulation, and endocrine resistance is critically discussed, together with current evidence describing the biological effects of selected phytochemicals including curcumin, epigallocatechin-3-gallate, resveratrol, sulforaphane, quercetin, and genistein. These compounds may influence prostate cancer-associated pathways through modulation of inflammatory signaling, oxidative stress, metabolic adaptation, chromatin remodeling, and microbiome dynamics. Major translational limitations including poor bioavailability, pharmacokinetic variability, microbiome heterogeneity, inconsistent clinical evidence, and incomplete mechanistic understanding are additionally discussed. Rather than considering natural products as isolated anticancer agents, this review adopts a systems-level perspective in which dietary bioactive compounds may function as modulators of interconnected regulatory networks relevant to prostate cancer biology and therapeutic responsiveness.

Achieving optimal therapeutic efficacy in colorectal cancer (CRC) remains challenging, highlighting the need for novel treatment strategies. This study evaluated whether radiofrequency (RF) hyperthermia enhances the anticancer effects of sunitinib malate and a newly synthesized tyrosine kinase (TK) inhibitor (compound 4). HCT116 CRC cells and BEAS-2B normal epithelial cells were treated with increasing concentrations of both agents in the presence or absence of RF exposure using a mobile RF device. Cell viability and death were assessed by MTT assay and flow cytometry (Annexin V/PI). RF exposure was associated with reduced viability and increased cell death in HCT116 cells (p < 0.05). Flow cytometric analysis confirmed that RF exposure may contribute to the observed reduction in viability. Notably, the findings suggest a possible beneficial contribution of RF hyperthermia to the observed cytotoxic effects, particularly near the IC50 concentration. In contrast, BEAS-2B cells maintained high viability with no significant changes (p > 0.05). These findings suggest that RF exposure may contribute to the observed cytotoxic responses in CRC cells while exerting limited effects on non-malignant cells, suggesting a promising strategy for targeted therapy.

Immune checkpoint inhibitors (ICIs) have transformed cancer therapy by restoring anti-tumor immunity, but immune activation can disrupt ocular immune homeostasis and induce ophthalmic immune-related adverse events (OirAEs). Although uncommon, OirAEs may involve nearly all ocular compartments and can cause irreversible visual impairment or interruption of effective anticancer therapy. The 2025 international consensus criteria now provide a standardized framework for defining and classifying OirAEs. This review integrates current evidence on ICI-associated ocular toxicity, with emphasis on tissue-specific immune mechanisms and their clinical implications. Blockade of the PD-1/PD-L1 and CTLA-4 pathways may impair ocular immune privilege, expand autoreactive T-cell subsets, alter cytokine and chemokine networks, and amplify autoantibody-mediated retinal injury. These processes provide a plausible framework for understanding diverse phenotypes, including uveitis, ocular surface disease, optic neuritis, orbital inflammation, ocular myopathy, and retinopathy. We also outline a mechanism-informed management approach that balances visual preservation with maintenance of systemic anti-tumor immunity. Local corticosteroid therapy, cautious systemic immunosuppression, and selected steroid-sparing biologics should be individualized according to severity, anatomical involvement, and the oncologic context. Together, these insights support a consensus-based and mechanism-informed framework for recognizing and managing OirAEs while preserving systemic anti-tumor immunity.

Pancreatic cancer remains a highly lethal malignancy, with standard therapies offering limited benefits in advanced stages; thus, novel strategies that exploit specific cancer cell vulnerabilities are urgently needed. Building on our previous findings that nanosecond pulsed electric fields (nsPEF) combined with cold atmospheric plasma (CAP) produce enhanced cytotoxicity, this study investigates the molecular mechanisms underlying this synergy. Pan02 pancreatic cancer cells were subjected to nsPEF, CAP, or a combination of both. We assessed cell viability, reactive oxygen species (ROS) production, and mitochondrial integrity using metabolic assays, flow cytometry, and fluorescence microscopy. Apoptotic markers were evaluated via Western blotting and caspase activity assays. Combined nsPEF-CAP treatment significantly outperformed either modality alone in inducing cell death. Mechanistically, dual treatment triggered a surge in intracellular ROS, particularly mitochondrial superoxide, indicating severe oxidative stress. Distinct mitochondrial responses were observed: nsPEF reduced mitochondrial membrane potential, whereas CAP alone caused a slight elevation. Notably, while CAP induced apoptosis (evidenced by increased cleaved caspase-3 and caspase-3/7 activity), lethal nsPEF (100 pulses) caused cell death without triggering apoptotic signaling. However, mild nsPEF (20 pulses) significantly potentiated CAP-induced apoptosis. These findings suggest that nsPEF sensitizes cells to CAP treatment by amplifying oxidative stress and mitochondrial dysfunction. This synergistic combination represents a promising therapeutic approach for managing pancreatic cancer cells resistant to conventional therapies.

Pancreatic cancer is among the most aggressive malignancies, and late diagnosis remains a key challenge. For a systematic review of pancreatic cancer diagnosis and prognosis, Scopus and Web of Science databases were used for the period from 2016 to 2026. The search query included the following keywords and their combinations: pancreatic cancer, diagnosis, early detection, prognosis, biomarkers, metabolomic profiling, CA19-9, microbiome, metagenomic changes, circulating tumor DNA, genomic analysis. Inclusion criteria included only articles published in English. Exclusion criteria included case reports and studies that did not examine pancreatic cancer. Our analysis demonstrates that integrating multi-omics data, particularly combining traditional CA19-9 with circulating tumor DNA (ctDNA) and metabolomic profiles (lipids, amino acids, carbohydrates), significantly improves diagnostic accuracy. Microbiome composition and genomic alterations further refine risk stratification and prognostic assessment. The synergistic use of these biomarkers may facilitate the development of screening, early diagnosis, risk stratification, and treatment optimization. However, the introduction of new diagnostic approaches into clinical practice requires additional verification, standardization and prospective clinical studies.

Dysregulation of ribosome biogenesis is increasingly recognized as a hallmark of tumor malignancy, yet its prognostic implications in lung adenocarcinoma (LUAD) remain incompletely characterized. This study aimed to construct a ribosome biogenesis-related prognostic model for LUAD and explore its potential relevance to the tumor immune microenvironment. Single-cell and bulk RNA sequencing data were integrated to identify ribosome biogenesis-related genes (RBRGs), from which a prognostic risk score was established via Cox regression, LASSO regression, and multivariate Cox analyses and validated in two independent GEO cohorts. Associations between the risk score and tumor mutation burden, immune infiltration, and computationally inferred immunotherapy response were systematically evaluated. In vitro experiments were performed to characterize the biological function of RPS19BP1, a key gene in the model. A total of 262 RBRGs were identified, and the derived 14-gene risk score demonstrated prognostic value across three cohorts (TCGA: 1-, 2-, 3-year AUC = 73.08, 72.44, 72.20; GSE68571: 1-, 2-, 3-year AUC = 67.93, 73.24, 77.59; GSE8894: 1-, 2-, 3-year AUC = 75.56, 72.99, 71.77). The low-risk group exhibited a more immunocompetent tumor microenvironment, whereas the high-risk group was associated with an immunosuppressive phenotype. Knockdown of RPS19BP1 significantly attenuated the proliferation, migration, and invasion of LUAD cells. This multi-omics-derived prognostic model showed prognostic potential in retrospective LUAD cohorts, is associated with distinct immune infiltration patterns, and identifies RPS19BP1 as a pro-oncogenic regulator in LUAD.

Chronic lymphocytic leukemia (CLL) is a genetically heterogeneous disease in which TP53 alterations represent major adverse prognostic factors; this study aims to describe the clinical implications of complex TP53 disruption in a rare case context. Molecular and cytogenetic profiling was performed using MLPA for copy number variations and targeted next-generation sequencing for mutation detection, following DNA extraction from peripheral blood and standardized bioinformatic analysis pipelines. The patient exhibited concomitant del(13q14) and del(17p13), alongside two pathogenic TP53 mutations, indicating functional inactivation of p53 and a high-risk genomic profile; despite this, treatment with a Bruton's tyrosine kinase inhibitor resulted in significant hematological improvement within six months. These findings highlight that adverse TP53 alterations override favorable cytogenetic markers and emphasize the necessity of comprehensive genomic testing to guide prognosis and personalized therapy in CLL.