Summaiya Khatoon

Obesity is a well-established risk factor for multiple cancers, and Metabolic Bariatric Surgery (MBS) has been associated with reduced cancer incidence and mortality. However, the molecular mechanisms underlying this risk reduction remain incompletely understood. Many recent transcriptomic, proteomic, and metabolomic studies have enabled system-wide molecular profiling following MBS. We performed a systematic analysis of publicly available MBS-related omics datasets, including transcriptomic ( n = 22), proteomic ( n = 6), and metabolomic studies ( n = 5), with pre- and post-operative comparisons. Comparative molecular analyses across all omics datasets were performed using Ingenuity Pathway Analysis (IPA). Sustained suppression of key oncogenic pathways, including Molecular Mechanisms of Cancer, Role of Tissue Factor in Cancer, and metastasis-associated signaling, was observed in tissue transcriptomic datasets (adipose, skeletal muscle, and gastrointestinal tract). In contrast, transcriptomic datasets predominantly showed immune remodeling, characterized by activation of innate immune pathways. Key molecular markers, including CCL2 , EGFL6 , and S100A8, were identified as consistently regulated across multiple datasets. Proteomic analyses revealed early postoperative suppression of inflammatory and acute-phase proteins, progressive downregulation of complement and coagulation cascades, and sustained upregulation of endocrine regulators such as sex hormone-binding globulin and extracellular matrix–stabilizing factors. Metabolomic profiling demonstrated significant alterations in amino acid, bile acid, and lipid metabolism following MBS. These molecular changes collectively reflect a shift toward a less inflammatory, hormonally balanced, and metabolically favorable systemic environment. These findings highlight the impact of MBS in inhibiting cancer-promoting biological processes and identify candidate molecular biomarkers for future translational and oncologic research.

Cancer remains a major global health challenge, consistently ranking as the second leading cause of mortality worldwide. Despite significant advancements in research and technology, the need to deepen our understanding of tumor biology and improve therapeutic strategies persists. This review focuses on the progress and challenges of four traditional cancer treatment modalities: surgery, chemotherapy, radiation therapy, and hormonal therapy. Surgery, the primary method for tumor removal, has evolved with the integration of fluorescence-based technology and robotic systems, enhancing precision and minimizing collateral damage. Radiation therapy has progressed with improved focus, intensity control, and 3D technology, refining both diagnosis and treatment. Chemotherapy has advanced from natural extracts to synthesized derivatives with amplified cytotoxicity against cancer cells. Hormonal therapy has emerged as a crucial strategy for hormone-dependent cancers, restraining growth or inducing regression. Despite these advancements, each approach faces ongoing challenges. Surgery struggles with complete tumor removal due to heterogeneity. Chemotherapy contends with drug resistance and side effects. Radiation therapy grapples with precision issues and limited access in some regions. Hormonal therapy faces resistance development and quality of life impacts. This study provides a comprehensive analysis of the evolution of these traditional anti-cancer therapies, offering insights into their progress and highlighting areas for future research. By examining these modalities, we aim to underscore their relevance in the current oncology landscape and identify opportunities for improvement in cancer treatment strategies.

Albumin-coated gold nanoparticles display potential biomedical applications, including cancer research, infection treatment, and wound healing; however, elucidating their interaction with normal cells remains an area with limited exploration. In this study, gold nanorods (GNR) were prepared and coated with bovine serum albumin (BSA) to produce GNR-BSA. The functionalized nanoparticles were characterized based on their optical absorption spectra, morphology, surface charge, and quantity of attached protein. The interaction between GNR-BSA and BSA with normal cells was investigated using human dermal fibroblasts. The cytotoxicity test indicated cell viability between ~63–95% for GNR-BSA over concentrations from 30.0 to 0.47 μg/mL and ~85–98% for BSA over concentrations from 4.0 to 0.0625 mg/mL. The impact of the GNR-BSA and BSA on cell migration potential and wound healing was assessed using scratch assay, and the modulation of cytokine release was explored by quantifying a panel of cytokines using Multiplex technology. The results indicated that GNR-BSA, at 10 μg/mL, delayed the cell migration and wound healing 24 h post-treatment compared to the BSA or the control group with an average wound closure percentage of 6% and 16% at 6 and 24 h post-treatment, respectively. Multiplex analysis revealed that while GNR-BSA reduced the release of the pro-inflammatory marker IL-12 from the activated fibroblasts 24 h post-treatment, they significantly reduced the release of IL-8 (p < 0.001), and CCL2 (p < 0.01), which are crucial for the inflammation response, cell adhesion, proliferation, migration, and angiogenesis. Although GNR-BSA exhibited relatively high cell viability towards human dermal fibroblasts and promising therapeutic applications, toxicity aspects related to cell motility and migration must be considered.