Search Results (17,700)

Cancer therapy-related cardiotoxicity has emerged as a major challenge in contemporary oncology, particularly in long-term survivors of childhood malignancies. Oxidative stress (OS)-induced cardiotoxicity represents a key mechanistic pathway underlying myocardial injury caused by numerous anti-neoplastic drugs, most notably anthracycline-based chemotherapy, while OS also critically contributes to radiotherapy-induced cardiotoxicity. Excessive reactive oxygen and nitrogen species generation promotes mitochondrial dysfunction, impaired calcium homeostasis, lipid peroxidation, endothelial injury, inflammatory activation, and cardiomyocyte apoptosis, ultimately leading to progressive cardiac remodeling and ventricular dysfunction. These processes are of particular concern in pediatric cancer survivors, especially children treated for leukemia, who face a substantially elevated lifetime risk of cardiovascular disease following treatment exposure. Increasing attention has, therefore, been directed toward nutritional strategies capable of modulating redox homeostasis and attenuating treatment-associated myocardial injury. Experimental and translational evidence suggests that selected dietary compounds and nutraceuticals, including polyphenols, omega-3 fatty acids, coenzyme Q10, selenium, antioxidant vitamins, nutrition-based epigenetic interventions and intestinal microbiota composition modulations may exert cardioprotective effects through preservation of mitochondrial integrity, enhancement of endogenous antioxidant defenses, and suppression of oxidative and inflammatory signaling pathways. Nevertheless, clinical implementation remains limited by insufficient standardization, heterogeneous study designs, and incomplete understanding of long-term efficacy and safety. This narrative review critically examines the molecular basis of the OS-induced cardiotoxicity and radiotherapy-induced cardiotoxicity and evaluates current evidence supporting nutrition-based cardioprotective interventions, with particular emphasis on pediatric leukemia survivors and the prevention of long-term cardiovascular complications following anticancer therapy. Full article

The discovery of ferroptosis and cuproptosis has significantly expanded the landscape of programmed cell death. Artesunate (ART), a semisynthetic derivative of artemisinin, exhibits pleiotropic pharmacological activities beyond its canonical antimalarial role, including anticancer and neuroprotective effects. However, a comprehensive review systematically integrating ART’s roles in modulating both ferroptosis and cuproptosis remains lacking. This review bridges this gap by synthesizing recent advances. The distinct core mechanisms of ferroptosis and cuproptosis are first outlined. Extensive evidence is then summarized regarding ART-induced ferroptosis in cancers, primarily through disrupting iron homeostasis (e.g., stabilizing transferrin receptor (TFRC), promoting ferritinophagy) and impairing antioxidant defenses (e.g., suppressing the System Xc⁻/ glutathione peroxidase 4 (GPX4) axis, targeting peroxiredoxins). In contrast, the anti-cuproptotic effect of ART is currently restricted to Parkinson’s disease (PD) models, mediated by the upregulation of astrocytic metallothionein 2A (MT2A) to chelate excess copper—the only validated cuproptosis-related mechanism of ART to date. The crosstalk between ferroptosis and cuproptosis at shared metabolic nodes, including glutathione depletion, mitochondrial dysfunction, and reactive oxygen species (ROS) amplification, is further delineated as a hypothesis-generating framework. This interplay suggests a theoretical potential for ART—when combined with functional nano-materials—to synchronously engage both death pathways, though direct experimental validation of such dual-pathway synergy for ART as a single agent remains lacking. Finally, translational prospects of ART in cancer therapy, neurodegenerative diseases, and hepatic fibrosis are discussed, together with current challenges and future directions. ART acts as a context-dependent modulator: pro-ferroptotic activity is evident across multiple disease models, whereas anti-cuproptotic activity is currently limited to PD and requires further validation. Systematic characterization of ART’s context-specific effects suggests a preclinical rationale for the future design of ART-based combination strategies targeting metal-dependent cell death, pending further validation. Full article

Breast cancer remains among the leading causes of incidence and mortality worldwide. Consequently, identifying new treatments and strategies is of critical importance. Evidence indicates that camptothecin and its derivatives may exert anticancer effects in various cancer cell lines, including colon, lung, and ovarian cancers. However, their effects in breast cancer are not yet fully understood. Prior theoretical studies employing docking and molecular dynamics suggest that camptothecin could bind to the HER2 and EGFR receptors, which are overexpressed in breast cancer cells. Investigating interactions between novel molecules with affinity for membrane receptors overexpressed in breast cancer is important for developing personalized therapies and for advancing strategies to selectively target nanomaterials to these cells for diagnostic and therapeutic purposes. This study evaluated the in silico and in vitro effects of camptothecin on the MCF-7 and MDA-MB-231 breast cancer cell lines. Our results show significant inhibition of proliferation and reduced migration at 24, 48, and 72 h in both cell lines. The theoretical analysis indicates high affinity of camptothecin for receptors overexpressed in breast cancer compared with current treatments. Full article

Background/Objectives: Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited targeted therapeutic options. Although the anticancer and pro-apoptotic properties of boswellic acids have previously been reported, the interaction profile of chemically defined β-boswellic acid (BA) with doxorubicin (DOX) remains insufficiently characterised in the murine 4T1 TNBC-like model. This study quantitatively evaluated BA–DOX drug interactions using different reference models and characterised the cytotoxic and apoptosis-associated cellular phenotype accompanying combined exposure. Methods: Cytotoxicity was assessed using the MTT assay and BA–DOX interactions were evaluated using the Chou–Talalay combination index (CI), highest single-agent (HSA) and Bliss independence models. Apoptosis and cell-cycle distribution were analysed by flow cytometry and mitochondrial membrane potential was assessed by JC-1 staining. Caspase-3/7 activity, RT-qPCR, live/dead Calcein-AM/PI staining, 4′,6-Diamidino-2-phenylindole (DAPI) nuclear staining, and cytokine measurements were also performed. Gene Ontology (GO), Kyoto Encyclopaedia of Genes and Genomes (KEGG), and STRING-based protein–protein interaction (PPI) analyses were used to explore putative molecular pathways associated with experimental findings. Results: The 48 h selectivity index of BA was 1.28, indicating only modest differential cytotoxicity between 4T1 cells and HaCaT keratinocytes under the experimental conditions rather than definitive cancer-cell selectivity. Drug-interaction analyses revealed concentration- and model-dependent effects, with the Chou–Talalay analysis indicating synergism in selected intermediate and higher concentration pairs. Under the selected phenotypic-characterisation condition, BA + DOX produced a greater apoptotic response than either single treatment, accompanied by increased G2/M and Sub-G1 fractions, mitochondrial membrane depolarisation, and increased caspase-3/7 activity. This treatment condition was not included in the drug-interaction analysis and was therefore not interpreted as a pharmacologically validated synergistic combination. RT-qPCR demonstrated increased mRNA expression of Bax, Casp3, and Casp9, decreased mRNA expression of Bcl2, and a marked increase in the Bax/Bcl2 mRNA ratio. Calcein-AM/PI and DAPI analyses further demonstrated increased cell death and apoptotic nuclear alterations. The measured concentrations of TNF-α and IL-6 in culture supernatants were lower after BA + DOX treatment, whereas IL-10 remained unchanged; however, these cytokine measurements were not normalised to viable cell number and therefore require cautious interpretation. Exploratory bioinformatic analyses identified predicted associations with apoptosis-, mitochondrial-, and cell-cycle-related processes and pathways; however, these database-derived findings were considered hypothesis-generating and not evidence of BA-dependent target engagement or pathway activation. Conclusions: Combined BA and DOX exposure produced greater cytotoxic and apoptosis-associated responses than either single treatment in 4T1 cells, whereas formal drug-interaction classifications varied according to concentration and analytical model. The accompanying changes in mitochondrial membrane potential, caspase-3/7 activity, and apoptosis-related gene expression describe a treatment-associated cellular phenotype but do not identify a direct molecular target of BA or establish a causal molecular mechanism. The findings also do not demonstrate TNBC-specific selectivity. Further studies using additional breast cancer and tissue-matched non-malignant models, together with direct target-engagement and functional pathway-validation approaches, are required. Full article

Background/Objectives: Rosmarinic acid (RA) is a naturally occurring polyphenolic compound with promising anticancer activity; however, its potential to enhance the therapeutic efficacy of doxorubicin (DOX) against triple-negative breast cancer (TNBC) has not been comprehensively characterised. This study investigated the pharmacological interaction and associated cellular responses of RA combined with DOX in MDA-MB-231 breast cancer cells, while including HaCaT human keratinocytes as a non-malignant, non-mammary reference model for comparative cytotoxicity assessment. Methods: Cell viability was assessed using the MTT assay, and pharmacological interactions were evaluated using Chou–Talalay combination index (CI) and dose reduction index (DRI) analyses. Intracellular oxidative activity was evaluated using DCFH-DA fluorescence analyses together with N-acetyl-L-cysteine (NAC) modulation experiments. Apoptosis, cell-cycle distribution, mitochondrial membrane potential (JC-1), Caspase-9 immunocytochemistry, nuclear morphology (NucBlue staining), apoptosis- and proliferation-related gene expression (RT-qPCR; BAX, BCL2, CASP3, CASP9, TP53, CDKN1A, MKI67, and PCNA), and bioinformatic pathway analyses were performed to characterise cellular and molecular responses associated with the combined treatment. Results: After 48 h, RA exhibited IC₅₀ values of 188.4 ± 4.2 µM in MDA-MB-231 cells and 146.6 ± 6.8 µM in HaCaT cells, while DOX showed IC₅₀ values of 1.2 ± 0.08 µM and 2.6 ± 0.15 µM, respectively. The Chou–Talalay analysis demonstrated synergistic interactions in MDA-MB-231 cells, with CI values of 0.86, 0.72, and 0.64 at the effect levels of IC₂₅, IC₅₀, and IC₇₅, respectively; the model-derived DOX DRI value at Fa = 0.50 was 1.8. Combination treatment markedly increased intracellular DCFH-DA fluorescence, whereas NAC pretreatment attenuated this signal and partially restored cell viability, supporting a contributory role of intracellular oxidative stress in treatment-associated cytotoxicity. Increased intracellular oxidative activity coincided with mitochondrial membrane depolarisation, increased apoptotic cell death, accumulation of cells in the sub-G₁ phase, enhanced Caspase-9 immunoreactivity, and pronounced apoptotic nuclear alterations. RT-qPCR analysis demonstrated significant upregulation of BAX, CASP3, CASP9, and TP53, together with downregulation of BCL2, MKI67, and PCNA, resulting in a marked reduction in the BCL2/BAX mRNA expression ratio. A modest but non-significant increase in CDKN1A expression was also observed. Bioinformatic analyses further identified predicted associations with mitochondrial apoptosis and p53-associated signalling pathways. Conclusions: The RA + DOX combination showed synergistic cytotoxic activity in MDA-MB-231 cells, accompanied by increased intracellular oxidative activity, mitochondrial membrane depolarisation, apoptosis, cell-cycle perturbation, and changes in proliferation-related gene expression. These findings indicate associated cellular responses but do not establish a ROS-dependent mitochondrial apoptotic mechanism. The findings provide an exploratory in vitro basis for further investigation of the RA + DOX combination in additional TNBC models, non-malignant mammary epithelial cells, and appropriate in vivo systems. Full article

Background: Retained totally implantable venous access ports (TIVAPs) pose a clinical management challenge after completion of intravenous anticancer therapy, particularly when future treatment needs remain uncertain. We aimed to characterize longitudinal post-treatment TIVAP trajectories after a day-90 conditional landmark, with elective removal prespecified as the primary first event. Methods: This retrospective cohort study included patients who were alive and event-free, retained the original TIVAP, had no documented TIVAP-related indication requiring removal, and had documented clinical and TIVAP status at day 90. Elective removal was the primary event; TIVAP reactivation, complication-related removal, and network-documented death were competing events. Results: Among 1406 patients, the 12-month cumulative incidence was 34.3% (95% confidence interval [CI], 31.4–37.1) for elective removal, 10.1% (95% CI, 8.2–11.9) for reactivation, 4.1% (95% CI, 3.0–5.3) for complication-related removal, and 1.0% (95% CI, 0.5–1.6) for network-documented death. During 1164.9 patient-years, 9978 maintenance-related patient-date encounters were recorded. In the assessed subcohort (n = 1319), 69.2% of assessments indicated willingness to choose a TIVAP again for similar future treatment, 64.4% indicated willingness to recommend TIVAP use, and 26.0% recorded a preference for earlier removal. Conclusions: Retained TIVAPs followed heterogeneous post-treatment courses, including elective removal, subsequent reuse, and continued retention requiring maintenance. These findings describe observed management patterns; they do not establish the comparative effectiveness of retention versus removal or identify an optimal removal time, and they support a prospective evaluation of structured reassessment pathways. Full article

Background: Breast cancer remains the most common malignant tumor among women worldwide. Although conventional treatments including surgery, chemotherapy, and radiotherapy are effective, they are confronted with challenges such as tumor heterogeneity, systemic toxicity, and recurrence driven by drug resistance. To overcome these limitations, natural products have emerged as promising therapeutic alternatives owing to their multi-target efficacy and favorable biocompatibility. However, their clinical translation is still hindered by poor chemical stability, low aqueous solubility, and inadequate bioavailability. Nanodelivery systems offer a transformative solution by enhancing bioavailability and enabling precision targeting through the enhanced permeation and retention effect, thereby widening the therapeutic window and minimizing off-target toxicity. Purpose: This review evaluates diverse nanoparticle-based delivery systems and their targeting mechanisms in natural product-based breast cancer therapy. By examining inherent advantages and translational challenges, this analysis provides critical insights into the clinical development and application of these nanoformulations. Methods: A systematic literature search was performed in PubMed, ScienceDirect, Springer, Taylor & Francis, and Web of Science to identify relevant studies on natural product-based nanoformulations for breast cancer therapy. Results: Natural products exert anti-breast cancer effects through mechanisms such as inducing apoptosis, arresting the cell cycle, inhibiting invasion and metastasis, suppressing angiogenesis, and regulating autophagy. To overcome clinical hurdles, three complementary targeting strategies have been developed: passive, active, and stimuli-responsive targeting. These advances are shifting nanomedicines toward active precision therapy, markedly improving the therapeutic index. With multiple formulations already approved or in clinical pipelines, this field is rapidly progressing from laboratory research to clinical implementation. Conclusions: Natural products possess potent anti-breast cancer effects, and the application of nanodelivery technology effectively overcomes their inherent limitations of poor stability and low bioavailability. Although preliminary findings are promising, large-scale, randomized controlled clinical trials are urgently needed to systematically evaluate their safety, efficacy, and practical potential for clinical translation in breast cancer management. Full article

Telomerase is an interesting biological target for cancer treatment. Despite recent advances in telomerase research and the rapid development of new methodologies, significant challenges remain in identifying effective telomerase inhibitors with anticancer activity. In this manuscript, we provide computational studies to analyse how structural modification of BIBR1532, a selective and non-competitive telomerase inhibitor, may affect binding by a newly reported human telomerase model. BIBR1532 has been extensively studied in various cancer types, but analyses have shown its low anticancer activity. Further modification of BIBR1532 yielded compound BIBR1591 through a lipophilic morpholine ring extension of the benzoic acid. Interestingly, BIBR1591 showed approximately five-fold weaker inhibitory activity toward human telomerase relative to BIBR1532, but its in vivo preclinical studies have demonstrated significant anti-tumour and pro-apoptotic efficacy. Despite promising preclinical activities, neither compound has advanced to clinical trials, reportedly due to challenges with its pharmacokinetic properties. BIBR1532 suffers from poor solubility and low cellular uptake. This manuscript aims to provide an updated overview of human telomerase inhibition by BIBR1532 analogues and emphasise the importance of understanding its molecular mode of action based on the most updated literature. Using an in silico approach, we analysed how the structural modification of the BIBR scaffold influences the binding mode at the BIBR binding site recently discovered in the structure of human telomerase. We have also assessed whether reported analogues offer a measurable advantage over the parent compound. Full article

MicroRNAs (miRNAs) are small non-coding RNAs that have emerged as critical regulators of gene expression and key cellular processes in cancer, including tumor cell proliferation, survival, metastasis, and both innate and adaptive immune responses within the tumor microenvironment. Through their ability to modulate immune cell development, differentiation, polarization, antigen presentation, cytokine signaling and immune checkpoint expression, miRNAs play a vital role in shaping immune responses and represent attractive therapeutic candidates for remodeling the tumor immune microenvironment. This review provides a comprehensive overview of the mechanisms through which miRNAs regulate anti-tumor immunity and contribute to immune evasion with particular emphasis on their role in modulating major immune checkpoint pathways, including PD-1/PD-L1, CTLA-4, LAG-3, TIM-3 and CD28-mediated signaling. We further examine the contribution of miRNAs to therapeutic resistance and discuss their potential integration with immune checkpoint blockade, chemotherapy, PARP inhibitors and targeted therapies to enhance antitumor efficacy and overcome treatment resistance. Recent advances in spatial transcriptomics and computational approaches have expanded our understanding of miRNA-mediated regulatory networks at single-cell and tissue levels and provide new insights into tumor–immune interactions. In addition, we evaluate the current progress in the clinical development of miRNA-based therapeutics, including miRNA mimics and inhibitors and discuss the major challenges associated with efficient delivery, off-target effects, immunogenicity and patient heterogeneity. Collectively, the evidence highlights the growing potential of miRNAs as diagnostic biomarkers, therapeutic targets and therapeutic tools in cancer immunotherapy. Continued advances in RNA therapeutics, delivery technologies and multi-omics approaches are expected to accelerate the clinical translation of miRNA-based strategies for personalized cancer therapy. Full article

Cancer remains a major global health concern, driving the search for safe and effective bioactive compounds from natural sources. Jujube peel red pigment (JP), an anthocyanin-rich extract, has shown preliminary bioactivity, yet its antitumor potential and delivery challenges remain underexplored. This study systematically evaluated the in vitro antitumor activity of JP and developed a thermosensitive hydrogel-based local delivery system (JP-H) to overcome its rapid diffusion and poor retention. JP exhibited selective cytotoxicity against HeLa cervical cancer and B16 melanoma cells, with no obvious toxicity to normal L929 and RAW264.7 cells. In HeLa cells, JP exerted antitumor effects by initiating mitochondrial-dependent apoptosis accompanied by elevated expression of Bax and cleaved Caspase-9/-3 as well as decreased Bcl-2 level, and arrested cell cycle at the G1/S phase by regulating CCND1, CDK2, CDK4, PCNA, MYC and TP53. To enable localized delivery, JP was incorporated into an injectable chitosan/gelatin/F127 thermosensitive hydrogel (JP-H), which exhibited rapid sol-gel transition at physiological temperature, shear-thinning behavior, and a porous microstructure. JP-H not only sustained JP release but also significantly enhanced antibacterial activity against E. coli and S. aureus compared to free JP. Furthermore, JP-H markedly inhibited HeLa cell migration and induced superior apoptotic/necrotic cell death in co-culture assays, outperforming free JP. Collectively, this work establishes JP as a multi-target antitumor agent and demonstrates JP-H as a promising local therapeutic platform combining sustained delivery, antibacterial protection, and enhanced anticancer efficacy for cervical cancer treatment. Full article

TPZ is a hypoxia-activated anticancer agent that exerts selective cytotoxicity within hypoxic tumor microenvironments. Although intratumoral injection of TPZ can achieve localized antitumor activity, the drug is prone to rapid diffusion and clearance from the injection site, limiting its long-term retention and thereby reducing therapeutic durability and overall efficacy. To achieve sustained release and prolonged retention of TPZ in subcutaneous tumors, a thermosensitive nanogel loaded with TPZ (TPZ@PNA-TNG) was developed. By thoroughly mixing 3 mg/mL TPZ with 6 wt% PNA-TNG, the resulting formulation enabled continuous slow release of TPZ following intratumoral injection, resulting in favorable therapeutic outcomes. The sol–gel phase transition behavior of TPZ@PNA-TNG was investigated using the inverted vial method and rheological measurements. In vivo antitumor studies demonstrated that a single administration of TPZ@PNA-TNG effectively suppressed tumor progression, with tumor volume decreasing to 0.72 ± 0.04 times its initial size over a 14-day period. Mechanistically, TPZ@PNA-TNG markedly enhanced antitumor immune responses, inhibited tumor cell proliferation, promoted apoptosis and anti-angiogenesis, and ultimately induced extensive ischemic necrosis within subcutaneous tumors. In addition, owing to the prolonged intratumoral retention capability of PNA-TNG, TPZ@PNA-TNG enabled sustained local delivery of TPZ, thereby significantly reducing systemic toxicity and adverse effects associated with TPZ while maintaining favorable biocompatibility. These findings highlight the therapeutic potential of TPZ@PNA-TNG for cancer therapy applications. Full article

Breast cancer [BC] is the most diagnosed cancer among women worldwide. Thanks to advancements in early detection, systemic therapies, and supportive care, survival rates have significantly improved. As more patients survive BC, cardiovascular disease [CVD] has emerged as a leading cause of long-term morbidity and mortality in this population. This is largely due to a combination of shared risk factors, such as obesity, diabetes and metabolic syndrome, combined to cardiotoxic effects of certain anticancer therapies, particularly anthracyclines, HER2-targeted therapies and radiotherapy. This review explores the cardiovascular [CV] implications of modern breast cancer treatments, including chemotherapy, endocrine therapy, targeted agents, radiotherapy, and emerging modalities such as immunotherapy. It also highlights the impact of patient-specific factors—such as diabetes, lipid profile, and treatment duration—on CVD risk. Current data suggest that breast cancer survivors are at increased risk of CVD compared to the general population, and that risk persists for years after treatment completion. CVD risk profile of each patient is different because of patient age, previous risk factors, and type of oncological treatment, and must be carefully delineated and keep well in mind during and after cancer treatment. Full article

Background and Objectives: Cancer-associated thrombosis (CAT) is still a leading cause of morbidity and mortality in patients with malignancy and represents a major challenge in cardio-oncology. Although low-molecular-weight heparins (LMWH) have long been the standard of care, direct oral anticoagulants (DOACs) have broadened treatment options. However, balancing thrombotic and bleeding risks, accounting for tumor- and individual-specific characteristics, requires an individualized therapeutic approach. This review summarizes current evidence supporting personalized anticoagulation strategies in CAT. Materials and Methods: A structured narrative review supported by a systematic literature search was conducted. Evidence regarding LMWH, DOACs, and emerging factor XI/XIa inhibitors was critically appraised, with emphasis on clinical scenarios necessitating individualized management, including gastrointestinal, genitourinary, and intracranial malignancies, hepatocellular carcinoma, thrombocytopenia, renal impairment, drug–drug interactions, and recurrent thrombosis. Results: Both LMWH and DOACs are effective options for CAT, with treatment selection guided by the balance between thrombotic and bleeding risks. Among DOACs, apixaban appears to have a favorable efficacy–safety profile based on current evidence, whereas rivaroxaban and edoxaban remain suitable for carefully selected patients despite higher bleeding risk in specific settings. LMWH continues to be preferred in patients with active mucosal tumors, severe thrombocytopenia, advanced renal dysfunction, significant drug–drug interactions, or when dosing flexibility is required. Emerging evidence also points to possible pleiotropic effects of DOACs on inflammation, angiogenesis, and metastatic progression, although the results have not yet translated into proven clinical benefit. Factor XI/XIa inhibitors remain investigational, with no established role in cancer-associated thrombosis. Conclusions: Contemporary CAT management has shifted toward personalized anticoagulant selection based on tumor characteristics, bleeding risk, organ function, anticancer therapy, and patient-related factors. Future advances, including factor XI/XIa inhibitors and a better understanding of anticoagulants’ biological effects beyond thrombosis prevention, may further optimize individualized treatment and improve clinical outcomes. Full article

Background: The emergence of oral anticancer medications (OAMs) has increased demand for specialized clinical pharmacy services (CPSs). Concurrently, Canadian cross-sectional data highlights undergraduate education gaps, with fewer than 14% of community pharmacists reporting adequate training on OAM therapies. We designed, implemented, and evaluated a pharmacist-led Oral Anticancer Medication Clinical Co-op Program (OAMCCP) to bridge this experiential education gap while cost-effectively expanding institutional capacity. Methods: Launched in Fall 2022, the OAMCCP integrated one PharmD student per 16-week term into a multidisciplinary oncology specialty pharmacy. Trainees executed core ambulatory oncology clinical pharmacy key performance indicators (AOcpKPIs), including Best Possible Medication Histories (BPMHs), drug–drug interaction (DDI) screenings, and proactive adherence and toxicity follow-up. Student competency was verified by a licensed oncology pharmacist to maintain patient safety. Impact was quantified via self-reported task logging over 15 weeks, standardized 10-point patient satisfaction surveys, payroll expenditure comparisons, and student testimonials. Results: Trainees completed 673 clinical tasks (~45 tasks/week), contributing 16.2 h of direct clinical support weekly—effectively adding +0.43 full-time equivalent (FTE) to service capacity. Mean patient satisfaction was 9.5/10 (n = 29), with students successfully managing inquiries in 96.5% of encounters. Financially, a 1.0 FTE student (44,700 CAD/year cost) captured clinical capacity valued at 69,300 CAD/year (0.43 FTE pharmacist equivalence). Conclusions: The OAMCCP resolves experiential training gaps while presenting a safe, scalable, and financially viable human resource framework that expands oncology pharmacy services. Full article

Geographical and botanical origin dominate the chemical composition and biological activity of propolis samples. In this study, thirty Turkish propolis samples collected from different regions within the Black Sea region were comprehensively evaluated to investigate the relationships between phytochemical composition, antioxidant capacity, antibacterial activity, and anticancer potential. The propolis samples were extracted using 70% aqueous ethanol and labeled as K1-K30. Total phenolic content (TPC), total flavonoid content (TFC), ferric reducing antioxidant power (FRAP), and DPPH radical scavenging activity were determined. Antibacterial activity was evaluated against both Gram-positive and Gram-negative bacterial strains using inhibition zone (ZI), minimum inhibitory concentration (MIC), and minimum bactericidal concentration (MBC) tests. Most of the extracts showed measurable antibacterial activity, where Gram-positive bacteria generally showed higher susceptibility compared to the tested Gram-negative bacterial species. The extracts K12, K13, K22, K24, and K28 demonstrated the strongest broad-spectrum antibacterial activity. Pearson correlation analysis revealed that antibacterial efficacy was more strongly associated with antioxidant capacity and flavonoid richness than with total phenolic content alone. FRAP and TFC emerged as the strongest predictors of antibacterial activity, while specific phenolic compounds (particularly quercetin and trans ferulic acid) were associated with enhanced activity against Gram-negative bacteria. Preliminary anticancer activity was assessed using cell viability assays at 24, 48, and 72 h. Cytotoxic responses were highly heterogeneous and strongly time-dependent. K10, among the extracts, exhibited the strongest anticancer activity, showing inhibition rates above 80% at 24 and 48 h, whereas K4 and K23 also demonstrated considerable cytotoxic effects. Notably, antibacterial and anticancer activities were not directly correlated. Extracts with strong antibacterial activity, such as K12 and K22, showed proliferative effects in anticancer assays, whereas K10 displayed weak antibacterial but strong anticancer activity. These findings demonstrate that antibacterial and anticancer properties of propolis are governed by distinct phytochemical compositions. Overall, this study highlights the multidimensional bioactivity of Turkish propolis and emphasizes the importance of comprehensive phytochemical characterization for identifying extracts with application-specific therapeutic potential. Full article