Thymoquinone (TQ), the active compound in Nigella sativa (black seed), has shown promising effects against cancer in many laboratory studies. In this review, we explore how TQ works on different aspects of cancer, from stopping cancer cell growth and spread, to triggering cancer cell death, reducing inflammation, and helping the immune system fight back. We also highlight how TQ may overcome one of the biggest problems in cancer treatment—chemoresistance. When used together with common treatments like chemotherapy, radiation, or immunotherapy, TQ has been shown to improve their effects and reduce harmful side effects in preclinical models. Our review further discusses how TQ affects cancer stem cells, the tumor environment, and gene regulation through epigenetics. While these findings are encouraging, the lack of human studies remains a major gap. We also address TQ’s limited absorption and suggest ways to improve its delivery in the body, such as using nanoparticles or other carriers. Through this review, we aim to show the wide-ranging potential of TQ as a natural compound that may help make cancer treatments more effective and better tolerated. We call for clinical studies to take this research further and bring TQ closer to use in real-world cancer care.

Background: Despite significant advancements in healthcare, the burden of stroke continues to rise in the developed world, especially during the COVID-19 pandemic. Association between COVID-19 infection and stroke is well established. Factors identified for the delay in presentation and management include a lack of awareness regarding stroke. We aimed to assess the general public knowledge and attitudes on stroke and stroke risk factors in the United Arab Emirates during the COVID-19 pandemic. Methods: A cross-sectional study was conducted between September 2021 and January 2022 among adults≥ 18 years old. Participants completed a self-administered questionnaire on sociodemographic characteristics and stroke knowledge and attitudes. Knowledge and attitude scores were calculated based on the number of correct responses. Linear regression analysis was performed to determine the factors related to knowledge and attitude towards stroke. Results: Of the 500 respondents, 69.4% were females, 53.4% were aged between 18 and 25, and nearly half were students (48.4%). The mean knowledge score was 13.66 (range 2-24). Hypertension (69%), smoking (63.2%), stress (56.4%) obesity/overweight (54.4%), and heart disease (53.6%) were identified as risk factors. Overall, the knowledge of signs/symptoms was suboptimal. The mean attitude score was 4.41 (range, 1-6); 70.2% would call an ambulance if someone were having a stroke. A monthly income of 11,000-50,000 AED and being a student were associated with positive knowledge. Being a non-health worker and lacking access to electronic media sources were associated with worse attitudes. Conclusion: Overall, we identified poor knowledge and suboptimal attitudes toward stroke. These findings reflect the need for effective public health approaches to improve stroke awareness, knowledge, and attitudes for effective prevention in the community. Presently, this is of utmost necessity, given the increased occurrence of stroke and its severity among COVID-19 patients.

Several randomized clinical trials have been undertaken to evaluate the effect of vitamin D supplementation on reducing the risk of cardiovascular disease (CVD) or CVD mortality; however, mixed results have been reported. The objective of this analysis is to quantify the effect of vitamin D supplements on CVD events and CVD mortality in adults. PubMed, the Cochrane Library and ClinicalTrial.gov were searched for randomized placebo-control trials on adults using common keywords related to vitamin D and CVDs. Two reviewers independently extracted data. The risk of bias was assessed using the Cochrane tool. Data analysis was done using Comprehensive Meta-Analysis V2 (Biostat, Englewood, NJ, USA) to calculate risk ratio (RR) and 95% confidence interval (95%CI). The systematic review and meta-analysis have been registered at PROSPERO (CRD42020165293). One thousand two hundred twenty four abstracts were retrieved, of which 9 (compromising 114 379 participants) were used. This analysis reveals that compared with placebo, vitamin D did not reduce any CVD events (RR = 0.95, 95%CI: 0.88–1.04), CVD mortality (RR = 1.04, 95%CI: 0.871–1.242), myocardial infarction event (RR = 0.96, 95%CI: 0.83–1.11), or myocardial infarction mortality (RR = 1.527, 95%CI: 0.828–2.816). Current evidence does not support the use of vitamin D for the prevention of major cardiovascular events. PROSPERO Registration Number: (CRD42020165293).

Cancer cells sustain rapid growth by reprogramming their metabolism to depend heavily on glycolysis, enhanced insulin signaling, and adaptive changes in the unfolded protein response (UPR). Insulin Potentiation Therapy (IPT) enhances the efficacy of chemotherapy by increasing insulin receptor expression, thereby improving the uptake of chemotherapeutic agents. Meanwhile, targeting endoplasmic reticulum (ER) stress disrupts the protein-folding machinery within cancer cells, steering them toward apoptosis. However, IPT faces several limitations, including limited clinical evidence, variable responses across tumor types, and concerns regarding safety and standardization. This review is the first to comprehensively examine the combined modulation of ER stress and IPT, highlighting novel clinical applications and presenting supporting evidence for this synergistic approach in cancer treatment. We compare the distinct metabolic features of cancer cells with those of normal cells and analyze how these differences contribute to tumor progression, the critical role of ER stress in cancer development, and the influence of insulin on cancer metabolism. In addition, we explore the potential synergy between IPT and ER stress modulation by delving into the mechanisms underlying IPT, the benefits of integrating ER stress modulation with IPT, and how insulin can modulate ER stress to improve therapeutic outcomes.

Metabolic reprogramming is central to cancer biology, enabling tumor cells to sustain rapid proliferation, resist stress, and adapt to therapy. However, these alterations are highly heterogeneous across cancer types, and current treatments rarely exploit subtype-specific metabolic vulnerabilities. To address this gap, we developed a unified bioinformatics framework that integrates transcriptomic profiling (UALCAN), drug–gene interactions (DGIdb), gene–disease associations (Open Targets), pathway enrichment (Enrichr), and protein–protein interaction networks (STRING/Cytoscape). This pipeline was applied to lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LSCC), breast cancer (BRCA), and metastatic breast tumors (MET500) to uncover cancer type–specific metabolic programs and prioritize translational targets. Our analysis revealed distinct signatures: LUAD showed glycolytic activation, LSCC coupled glycolysis with oxidative phosphorylation, BRCA favored anabolic and lipogenic pathways, and MET500 tumors adopted stress-adaptive states with elevated antioxidant and autophagy programs. Integration of pharmacological evidence highlighted clinically actionable interactions between metabolic genes and FDA-approved drugs, including ASNS–asparaginase, DHODH–teriflunomide, and G6PD–rasburicase. Gene–disease associations further prioritized G6PD, SLC2A1, and TK1 as robust targets strongly linked to lung and breast cancers. Pathway enrichment pinpointed the pentose phosphate pathway, pyrimidine metabolism, and glutathione metabolism as conserved axes sustaining tumor survival, while network analysis positioned the G6PD–PGD hub as a central metabolic node connecting glucose uptake, redox balance, and nucleotide biosynthesis. To place these bioinformatics-derived findings within a functional and clinical context, we complemented the computational analyses with patient survival assessment, clinical trial screening, and targeted literature appraisal. Survival analysis demonstrated cancer type–specific prognostic relevance for selected metabolic genes, while clinical and literature-based screening revealed both ongoing translational efforts and substantial gaps between computational target prioritization and experimental or clinical validation. This integrative analysis shows that cancer metabolism is altered in subtype-specific ways that can be systematically mapped to reveal potential therapeutic targets. By linking transcriptomic evidence with drug–gene interactions and clinical context, this framework provides a scalable approach for cancer metabolism research and supports the prioritization of pathways with potential translational relevance.

Manganese (Mn)-based metal-organic architectures offer a unique avenue for integrating magnetic resonance imaging (MRI) and cancer therapy within a single molecular platform. We report three topologically distinct Mn-templated structures─Mn-[2]Catenate (Mn-[2]C), Mn-Trefoil Knot (Mn-TK), and Mn-Borromean Rings (Mn-BR)─that combine high relaxivity with tumor-selective cytotoxicity. The design leverages their geometrical complexity and electropositive, pH-labile coordination framework to ensure kinetic stability and lipophilicity at physiological pH while enabling Mn²⁺ release in the acidic tumor microenvironment. Among the three, Mn-BR and Mn-TK exhibit superior longitudinal relaxivities (r₁ = 10.1 and 6.8 mM^-1.s^-1 at 3 T) and produce bright T₁-weighted contrast exceeding that of Gd-DTPA and Mn-DPDP. In vitro, they show high cancer selectivity and potency in glioblastoma (U251-MG) cells, with IC₅₀ values of 3.0 ± 0.9 μM (Mn-BR) and 5.6 ± 1.9 μM (Mn-TK), outperforming cisplatin (12.7 ± 2.5 μM) while sparing normal cells (SI > 3.9 for Mn-TK; SI > 9.4 for Mn-BR). Mechanistically, their uptake proceeds via energy-dependent endocytosis─caveolae-mediated for Mn-TK and clathrin/macropinocytosis-driven for Mn-BR─culminating in lysosomal acidification, pH-triggered disassembly, Mn²⁺ release, ROS accumulation, and caspase-dependent apoptosis. In vivo, Mn-TK and Mn-BR achieve tumor-specific accumulation, strong MRI contrast, and pronounced growth inhibition in subcutaneous glioblastoma models, while Mn-[2]C shows minimal selectivity and higher systemic toxicity. Importantly, in a spontaneous orthotopic glioblastoma model, both Mn-TK and Mn-BR provided robust BBB permeability and persistent, tumor-specific MRI enhancement, confirming their potential for precise MRI-guided tumor visualization. This research marks a major leap forward in medical nanotechnology, unveiling a new class of metal-organic structures that seamlessly integrates imaging and therapy. By unlocking their full potential, these structures promise to revolutionize MRI diagnostics, precision medicine, and next-generation cancer treatments, paving the way for unparalleled clinical outcomes.