REVIEW ARTICLE | April 7, 2026
Cancer as a Systems Biochemical Disease: Multi-Omics Integration of Metabolomics, Proteomics, and Epigenomics
Muhammad Sajid Saleem, Eisha Habib, Muhammad Umar Farooq, Hajra Ibrahim, Fatima Hidayat, Suneel Kumar
Page no 236-247 |
https://doi.org/10.36348/sjls.2026.v11i04.001
Cancer is now being viewed not as a single genetic disease but as a multi-layered, multi-level disease that exists on a systems level and is a biochemical process that is powered by dynamic, multi-layered interactions with molecules. This review will take the systems biology approach by combining metabolomics, proteomics, and epigenomics to explain the biochemical heterogeneity and adaptive plasticity of cancer. The bioenergetic requirements of growing tumor cells are manifested through metabolomic reprogramming which is the altered glycolysis, lipid metabolism, and redox balance. Simultaneously, proteomic changes remodel signaling pathways, which mediate cell survival, immune resistance, and treatment resistance. Additional epigenomic changes such as DNA methylation, changes in histone positioning and regulation of non-coding RNAs also coordinate the pattern of gene expression without changing the sequence of the DNA itself. The intersection of these layers of omics points to cancer as an outcome of interdependent biochemical processes, and not single events at the molecular level. Recent developments in the field of multi-omics integration, which has been made possible by the high-throughput and computational modeling technologies, have allowed the discovery of new biomarkers and therapeutic targets with greater specificity and predictive capability. Notably, this integrative model changes the existing paradigm of reductionist approaches to the holistic tumor biology concept. This review identifies the opportunity of systems-level knowledge in informing precision oncology by mapping cross-talk between metabolic pathways, protein networks, and epigenetic landscapes. Finally, the combination of multi-omics information offers a strong foundation to unlock the complexity of tumors, enhance the early diagnosis of cancer, and inform the design of tailored therapeutic approaches during cancer treatment.
Functional nutrition plays a pivotal role in aquaculture by promoting fish growth, enhancing immune responses, and mitigating the impact of environmental and pathogenic stressors. With the intensification of fish farming and growing concerns over antibiotic resistance, the use of functional feeds including nutraceuticals, prebiotics, probiotics, antioxidants, and immunostimulants has emerged as a sustainable alternative to conventional practices. This review critically examines the nutritional requirements of fish, explores the bio efficacy of various feed additives, and evaluates their roles in gut health modulation, disease resistance, and stress mitigation. We also discuss proactive health management strategies and the integration of vaccination and feed-based interventions. The review highlights current advancements, identifies research gaps, and emphasizes the need for precision in formulating functional feeds tailored to species-specific requirements. This integrated nutritional approach supports healthier fish stocks, improves aquaculture productivity, and reduces the industry's ecological footprint.
Nickel sulphate (NiSO4) is a common industrial substance employed in various applications such as electroplating, battery production, and metal coating. However, its continuous occupational and environmental exposure has elicited toxicological issues. This review is a critical assessment of the histopathological, biochemical and molecular alterations of the liver in mice exposed to nickel sulphate, correlating the findings from both animal and mechanistic tests. Studies evidently show that NiSO4 leads to dose-related liver cell damage, necrosis, steatosis, inflammatory infiltration, and degeneration in animals, closely linked to the increase of serum transaminases and oxidative-stress biomarkers. From a mechanistic perspective, nickel exposure affects redox homeostasis, mitochondrial integrity, and lipid metabolism leading to ferroptosis, apoptosis, and endoplasmic reticulum stress signalling. Additionally, comparative data analysis between hepatic injuries induced by soluble and particulate nickel salts shows that the former is more fatal, highlighting the relevance of compound bioavailability and exposure pathway. The hepatoprotective effects of antioxidants and flavonoid supplements (e.g. selenium, silymamarin, hesperidin, etc.) against hepatic injury are seen in preclinical models. Cross-species researchers also show that there are conserved oxidative and inflammatory systems of damage, suggesting it may be applicable in human risk assessment. According to the review, early biomarkers, multi-omics, and mechanistically directed interventions are needed to enhance toxicological assessment. Overall, long-term exposure to nickel sulphate is a realistic risk for hepatic damage; therefore, increased occupational preventive and mechanistic research should be used to improve preventive and therapeutic strategies.