Introduction: Interindividual variability in cancer therapy response cannot be fully explained by host genetics or tumor characteristics alone. Emerging evidence indicates that the gut microbiome is a critical modulator of anticancer drug metabolism, immune responses, and therapeutic outcomes, positioning it as an important determinant in cancer pharmacology. Methods: This narrative review employed a structured literature search of PubMed, Scopus, and Web of Science (2005-2025) to synthesise preclinical and clinical evidence on microbiome-drug interactions, focusing on pharmacokinetics, immune modulation, toxicity, and resistance across chemotherapy, immunotherapy, and targeted therapies. Results and Discussion: The gut microbiome influences anticancer therapy through enzymatic biotransformation, immune regulation, metabolite signalling, and maintenance of intestinal barrier integrity. Clinically, favourable microbiome profiles have been associated with improved immunotherapy outcomes, with reported hazard ratios for survival ranging from ~0.5 to 0.7, while prior antibiotic exposure is linked to a 20-40% reduction in response rates. Microbial enzymes such as β- glucuronidase contribute to irinotecan-induced toxicity, affecting up to 20-40% of patients. Specific taxa, including Akkermansia muciniphila and Bifidobacterium spp., are associated with enhanced therapeutic response. Microbiome-targeted interventions, including faecal microbiota transplantation, have demonstrated response restoration in approximately 30-40% of refractory cases in early clinical studies. However, heterogeneity in microbial composition, lack of standardisation, and safety concerns limit clinical translation. Conclusion: The gut microbiome represents an adaptable determinant of cancer pharmacology. Integrating microbiome-informed strategies offers a promising pathway toward precision oncology, although robust clinical validation remains essential for routine implementation.

The separation and quantitative determination of polar and ionic compounds remain among the most persistent and technically demanding challenges in analytical chemistry. Such analytes encompass a w...

Introduction: Arsenic is a ubiquitous environmental metalloid with dual characteristics-acting as both a potent toxin and an effective therapeutic agent. Chronic exposure to inorganic arsenic species, arsenite [As(III)] and arsenate [As(V)], is associated with multiple cancers and systemic diseases, whereas Arsenic Trioxide (ATO) demonstrates strong anticancer efficacy, particularly in Acute Promyelocytic Leukemia (APL). Methods: A systematic literature search was conducted across PubMed, Scopus, Web of Science, and Google Scholar to review epidemiological, experimental, and clinical studies. Inclusion criteria focused on works addressing arsenic-induced genotoxicity, proteotoxicity, and therapeutic applications. Data were extracted regarding molecular mechanisms, biomarkers, and mitigation strategies. Results: Arsenic induces oxidative stress, DNA damage, and epigenetic alterations, leading to genomic and proteomic instability. Clinical evidence indicates ATO achieves remission rates exceeding 90% in APL by degrading the PML-RARα oncoprotein. Emerging nanotechnology and precision medicine approaches enhance drug delivery, reduce systemic toxicity, and support targeted therapy. Discussion: Arsenic’s paradoxical behavior is dose- and context-dependent. While chronic lowlevel exposure drives carcinogenesis, controlled pharmacologic use offers therapeutic benefit. Integration of omics technologies and nanocarriers can refine their safety and clinical applicability Conclusion: Arsenic exemplifies the intersection of toxicity and therapy. Understanding its genotoxic and proteotoxic mechanisms supports the development of safer, precision-based interventions and expands its potential as a therapeutic agent in modern oncology

Introduction: Metabolomics, utilizing sophisticated analytical platforms such as mass spectrometry (MS), is critical for uncovering diagnostic and prognostic cancer biomarkers. This review highlights cutting-edge analytical techniques and their role in biomarker discovery for early detection, prognosis, and therapeutic monitoring, focusing on lung, breast, bladder, prostate, and ovarian cancers. Methods: This review was conducted using studies published over the last five years from PubMed, Scopus, Web of Science, and Google Scholar. Inclusion criteria focused on advanced metabolomics platforms, specifically Nuclear Magnetic Resonance (NMR), Gas Chromatography– Tandem Mass Spectrometry (GC-MS/MS), Capillary Electrophoresis–Tandem Mass Spectrometry (CE-MS/MS), and Liquid Chromatography–Tandem Mass Spectrometry (LCMS/ MS), for cancer biomarker identification. Results: Emerging technologies and automated workflows have substantially improved metabolite detection, quantification, and interpretation. These innovations have facilitated the discovery of distinct metabolic signatures associated with tumor progression and drug resistance. Integration with systems biology has further supported the development of non-invasive diagnostic and prognostic tools. Discussion: Advanced analytical techniques, including MS and NMR, are transforming precision oncology through robust biomarker discovery. However, challenges such as the complexity of cancer metabolic pathways, inter-sample variability, and the lack of standardized protocols remain significant barriers to clinical translation. Conclusion: Future developments, particularly multi-omics integration and real-time metabolite monitoring, are expected to enhance the clinical utility of metabolomics, paving the way for its full integration into personalized cancer diagnosis, prognosis, and therapy.

Introduction: A combination of environmental variables, a genetic background, and exposure to sunlight is causing the rate of skin cancer to rise worldwide. The most often diagnosed cancers are non-melanoma skin cancers, especially cancers of the squamous cells (SCC) and basal cell carcinoma (BCC). Although aggressive and surgical therapies are successful, they frequently cause relapse, impairment in functioning, or scarring. A less intrusive option with good cosmetic results is photodynamic treatment (PDT), which uses a light-activated photosensitizer to generate reactive oxygen species (ROS). The purpose of this study is to provide an overview of the mechanisms, developments, efficacy in clinical settings, and constraints of PDT in the treatment of skin cancer. Methods: The databases PubMed, Scopus, Web of Science, and Google Scholar were used to do a narrative review of the literature. "Photodynamic therapy", "the skin cancer", photosensitizers", and "nanotechnology" were among the phrases used. To assess PDT mechanisms, pigment development, clinical outcomes, and new technical tactics, Englishlanguage peer-reviewed literature, research, and review studies were examined. Results: PDT offers superior cosmetic outcomes and selective tumor eradication for actinic keratosis, intermediate BCC, and initial SCC. Tumor hypoxia, uneven photosensitizer absorption, and limited penetration into the tissues are some of the associated limitations. The precision of therapy has been strengthened by recent developments in nanocarrier systems, advanced photosensitizers, and efficient light-delivery methods. In order to overcome resistance and improve medical response, mixed methods that incorporate PDT with immune therapy, chemotherapy, or biological strategies show possibility. Discussion: PDT's growing use in dermatological oncology has been reinforced by its tailored activity and advantageous aesthetic profile. Treatment of deeper or malignancies caused by still presents difficulties, necessitating the use of improved exposure systems, near-infrared photosensitizers, and nanotechnology. Multiple therapies may improve effectiveness even more and lower the chance of reappearance. Conclusion: PDT is a cutting-edge, successful treatment for superficial skin cancers. It is anticipated that collaborative treatment approaches and technological advancements would increase its practical utility and enhance patient results and quality of life.

Antimicrobial resistance (AMR) poses a significant threat to global public health and economic stability, driven by the overuse and misuse of antibiotics in human medicine, veterinary practice, and agriculture. The spread of resistance mechanisms, such as enzymatic degradation, efflux pumps, and horizontal gene transfer, further exacerbates this issue, particularly in low-resource settings. This review aims to summarize the current understanding of antimicrobial resistance, including its molecular mechanisms, global challenges, economic burden, and innovative mitigation strategies such as antimicrobial stewardship, phage therapy, antimicrobial peptides, and CRISPR-based approaches. A comprehensive literature review was conducted using scientific databases such as PubMed, Scopus, and Web of Science to gather recent studies, reviews, and guidelines related to AMR. Relevant data on resistance mechanisms, global trends, clinical implications, and mitigation strategies were synthesized to provide an integrated overview of current challenges and solutions. The review highlights how AMR contributes to increased mortality, prolonged illness, and healthcare costs, while barriers such as limited antibiotic research and diagnostic capacity hinder progress. Integrated approaches, including antimicrobial stewardship, vaccination, phage therapy, and CRISPR-based therapies, are essential to reduce resistance. Additionally, global initiatives like surveillance systems and public awareness campaigns play a vital role in controlling the spread of resistant infections. Addressing AMR requires coordinated global efforts involving stewardship programs, novel therapeutics, education, and surveillance systems. Sustainable action can reduce antibiotic misuse and delay resistance development, securing effective treatments for future generations.