Oral cancer, particularly oral squamous cell carcinoma (OSCC), remains a leading cause of cancer-related morbidity and mortality, with delayed diagnosis being a major contributing factor. Although salivary biomarkers have been explored for over three decades, the need for reliable, non-invasive diagnostic methods that enable early detection and continuous monitoring of OSCC remains unmet. This review aims to provide an updated overview of the latest advancements in salivary biomarker research, focusing on emerging biomarkers such as interleukin-6, interleukin-8, microRNAs and DNA methylation patterns, as well as metabolites and microbiota, all of which show significant promise for early OSCC detection. In addition to discussing well-established biomarkers, we explore recent technological developments that increase the sensitivity and specificity of these biomarkers, such as mass spectrometry, multiplex assays, and nanobiosensors. These developments are complemented by the integration of artificial intelligence for data analysis, which enables more accurate, point-of-care diagnostics that could revolutionize oral cancer screening. This review not only consolidates current knowledge but also addresses the challenges that hinder the widespread clinical adoption of salivary diagnostics, such as saliva variability and assay standardization. By overcoming these barriers, salivary biomarker-based diagnostics have the potential to transform OSCC detection, offering a non-invasive, cost-effective solution that can improve early diagnosis and patient outcomes.

Liver cancer, particularly hepatocellular carcinoma (HCC), remains a significant global health challenge due to its high mortality rate and late-stage diagnosis. The discovery of reliable biomarkers is crucial for improving early detection and patient outcomes. This review provides a comprehensive overview of current and emerging biomarkers for HCC, including alpha-fetoprotein, des-gamma-carboxy prothrombin, glypican-3, Golgi protein 73, osteopontin, and microRNAs. Despite advancements, the diagnostic limitations of existing biomarkers underscore the urgent need for novel markers that can detect HCC in its early stages. The review emphasizes the importance of integrating multi-omics approaches, combining genomics, proteomics, and metabolomics, to develop more robust biomarker panels. Such integrative methods have the potential to capture the complex molecular landscape of HCC, offering insights into disease mechanisms and identifying targets for personalized therapies. The significance of large-scale validation studies, collaboration between research institutions and clinical settings, and consideration of regulatory pathways for clinical implementation is also discussed. In conclusion, while substantial progress has been made in biomarker discovery, continued research and innovation are essential to address the remaining challenges. The successful translation of these discoveries into clinical practice will require rigorous validation, standardization of protocols, and cross-disciplinary collaboration. By advancing the development and application of novel biomarkers, we can improve the early detection and management of HCC, ultimately enhancing patient survival and quality of life.

Curcumin, a polyphenolic compound derived from the turmeric rhizome (Curcuma longa), has attracted significant interest in dentistry and oral medicine because of its multifaceted therapeutic properties. In particular, curcumin exhibits potent anti-inflammatory, antioxidant, and antimicrobial activities that are relevant to a wide spectrum of oral diseases. We conducted a narrative search of PubMed (2000–2025) using iterative keyword combinations related to curcumin and oral diseases/mechanisms, screened reference lists, and selected studies on the basis of their relevance to oral pathobiology, delivery systems, and clinical/translational outcomes. This narrative review summarized the current knowledge concerning the molecular mechanisms of curcumin and its clinical applications in oral health. We outlined how curcumin modulates key inflammatory pathways and oxidative stress responses, and how it exerts broad-spectrum antimicrobial effects against oral pathogens. We detailed the efficacy of curcumin in specific oral conditions, including periodontal diseases, dental caries, recurrent aphthous stomatitis, oral lichen planus, oral submucous fibrosis, oral candidiasis, radiation/chemotherapy-induced oral mucositis, and oral cancers. In each context, we highlighted evidence from in vitro studies, animal models, and clinical trials, and noted the benefits of curcumin, such as reduced inflammation, enhanced healing, microbial inhibition, and in some cases outcomes comparable to those of standard therapies. Across conditions, curcumin shows adjunctive benefit: In periodontal disease, it reduces plaque and gingival inflammation comparable to chlorhexidine and improves probing outcomes when added to scaling and root planing; in recurrent aphthous stomatitis, it reduces pain and ulcer size with steroid-like efficacy; in radiotherapy/chemotherapy-induced oral mucositis, it delays onset and decreases severity; in oral candidiasis, it decreases fungal burden and enhances photodynamic therapy; and in oral squamous cell carcinoma early clinical studies show modulation of inflammatory cytokines and the oral microbiome. Various delivery systems developed to overcome the poor bioavailability of curcumin—from mouthwashes and gels to nanocarriers and mucoadhesive formulations—are reviewed. Although many studies reported promising results with minimal toxicity or side effects, there were study limitations such as small sample sizes, variability in formulations, and the pharmacokinetic properties of curcumin. Overall, the reviewed data support the role of curcumin as a safe, formulation-dependent adjunct—not a stand-alone therapy—in oral medicine.

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most challenging malignancies, with poor survival rates due to late-stage diagnosis and limited treatment options. Neoadjuvant therapy (NAT), which involves chemotherapy or chemoradiation prior to surgical resection, has emerged as a promising approach to improve resectability and overall survival (OS). The integration of advanced imaging techniques and biomarkers for evaluating the response to NAT is crucial for optimizing therapeutic strategies and surgical outcomes. However, challenges related to the heterogeneity of treatment protocols and the need for predictive biomarkers remain, highlighting the necessity for further clinical trials. The aim is to evaluate the impact of NAT on surgical outcomes and predictive markers in pancreatic cancer. A comprehensive review of the literature was conducted to evaluate the impact of NAT on surgical resectability, survival outcomes, and the role of imaging and biomarkers in assessing therapeutic response. Studies examining the efficacy of NAT in patients with PDAC, the predictive value of serum biomarkers such as carbohydrate antigen 19-9 (CA 19-9), and the utility of advanced imaging modalities such as positron emission tomography/computed tomography with 18F-fluorodeoxyglucose (FDG-PET/CT) were included. NAT has demonstrated significant benefits in downstaging tumors, increasing margin-negative (R0) resection rates, and reducing micrometastatic disease. The use of serum CA 19-9 Levels as a biomarker for response evaluation and imaging modalities such as FDG-PET/CT and magnetic resonance imaging has proven valuable in predicting therapeutic efficacy and guiding surgical planning. Studies have shown that significant reductions in CA 19-9 Levels and favorable metabolic responses on imaging are associated with higher R0 resection rates and longer survival. Furthermore, the integration of multimodal imaging and biomarker assessment has enabled better stratification of patients and more personalized treatment strategies. NAT significantly improves surgical outcomes and survival in patients with resectable and borderline resectable PDAC. Advanced imaging techniques and biomarkers such as CA 19-9 play pivotal roles in evaluating the response to therapy and guiding surgical decision-making. Future research should focus on addressing variability in treatment strategies and developing more reliable predictive biomarkers.

Interleukin-33(IL33), an alarm cytokine of the IL-1 family, is expressed mainly in epithelial cells of barrier tissues and is involved in the repair of epithelia to maintain barrier function. However, the mechanisms regulating IL33 expression and the mechanisms by which IL33 regulates the intestinal barrier function are not fully clarified. In this study, Caco-2 cells and siRNA were applied to investigate the role of Notch/IL33/ST2 Signaling in regulating intestinal epithelial barrier function, which was demonstrated by protein expression of tight junctions and trans-epithelial resistance (TER) assay. Our results revealed that Notch signaling pathway was activated and IL33 expression was up-regulated after LPS stimulation. After blocking Notch signaling with DPAT or siRNA for Notch1, IL33 expression was significantly down-regulated in Caco-2 cells. The protein expression of tight junctions (ZO-1, occludin, and claudin-1) was down-regulated after siRNA for IL33 in Caco-2 cells with LPS stimulation. Also, the intestinal epithelial TER was down-regulated after siRNA for IL33 with LPS stimulation or not. Exogeneous IL33 promoted the tight junction protein expression and increased the TER. Finally, our data further showed that IL33 regulates intestinal epithelial barrier function through the ST2 receptor. In conclusion, our results indicated that IL33/ST2 axis, which was activated by the Notch signaling, maintains intestinal epithelial barrier function through regulating tight junction protein expression under inflammatory conditions. This study provides a new therapeutic pathway of regulating intestinal epithelial barrier dysfunction.