With the rapid development of artificial intelligence (AI) technology, multimodal data integration has become an important means to improve the accuracy of diagnosis and treatment in gastroenterology and hepatology. This article systematically reviews the latest progress of multimodal AI technology in the diagnosis, treatment, and decision-making for gastrointestinal tumors, functional gastrointestinal diseases, and liver diseases, focusing on the innovative applications of endoscopic image AI, pathological section AI, multi-omics data fusion models, and wearable devices combined with natural language processing. Multimodal AI can significantly improve the accuracy of early diagnosis and the efficiency of individualized treatment planning by integrating imaging, pathological data, molecular, and clinical phenotypic data. However, current AI technologies still face challenges such as insufficient data standardization, limited generalization of models, and ethical compliance. This paper proposes solutions, such as the establishment of cross-center data sharing platform, the development of federated learning framework, and the formulation of ethical norms, and looks forward to the application prospect of multimodal large-scale models in the disease management process. This review provides theoretical basis and practical guidance for promoting the clinical translation of AI technology in the field of gastroenterology and hepatology.

This article reviews the mechanisms by which marine natural products regulate ferroptosis and their potential applications in tumor therapy. Ferroptosis is a form of programmed cell death driven by iron-dependent lipid peroxidation, characterized primarily by the accumulation of lipid peroxides and the failure of antioxidant defense systems. Due to their unique chemical structural diversity, marine natural products demonstrate significant advantages in regulating the ferroptosis pathway. Studies showed that marine compounds target key molecules such as glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthetase 4 (ACSL4(a)) ACSL4(1) to modulate lipid peroxidation and iron metabolism, inducing ferroptosis in tumor cells and reshaping the tumor microenvironment (TME). In addition, marine compounds can enhance anti-tumor effects by activating immune responses. Although marine compounds hold great potential in regulating ferroptosis, their clinical translation faces challenges such as low bioavailability and tumor type dependency. Future research needs to integrate multi-omics techniques to further analyze the mechanisms of marine compounds and develop precision therapeutic strategies based on marine compounds to overcome the bottlenecks in ferroptosis therapy.

Tumor organoid models are revolutionizing cancer research by bridging the translational gap between conventional two‐dimensional cell cultures and animal models. This Editorial thoroughly explores the fundamental innovations of patient‐derived organoid technology. Firstly, it achieves highly physiologically relevant disease modeling by preserving the genetic heterogeneity and microenvironmental complexity of patient tumors. Secondly, it uniquely integrates microfluidic chips, artificial intelligence, and single‐cell multi‐omics analysis to facilitate high‐throughput drug screening and accurate efficacy prediction. Thirdly, it has significantly advanced the development of immune co‐culture models and the study of tumor–immune interactions, offering a novel platform for examining immune therapy resistance mechanisms. The paper also critically assesses the current challenges in clinical translation, such as the lack of standardization and the complexity of vascular network reconstruction, and suggests future directions focusing on “organoid biobanks” and multicenter clinical validation. This Editorial not only systematically discusses the technological evolution but also provides a theoretical framework and practical path for transitioning organoids from basic research to clinical decision‐making, thereby ushering in a new era of precision cancer medicine.

SUMOylation is a dynamic and reversible post‐translational modification that has evolved from a regulator of fundamental cellular processes to a key driver of tumorigenesis and progression. By centering on three core pathological dimensions, namely aberrant cell death, metabolic reprogramming, and immune microenvironment dysfunction, this review systematically elucidates how SUMOylation orchestrates malignant tumor progression through these interconnected axes. It provides a detailed overview of the SUMOylation enzymatic cascade, its regulatory features including dynamics, substrate specificity, and responsiveness to cellular stress, and its complex crosstalk with other modifications such as ubiquitination and phosphorylation, which together enable precise and context‐dependent functional outcomes in various cancers. A distinctive aspect of this review is its integration of mechanistic insights with emerging therapeutic strategies, evaluating the translational potential of targeting the SUMO pathway, highlighting opportunities to overcome drug resistance and modulate antitumor immunity, while also addressing current challenges in clinical development. In contrast to most existing reviews that follow a trajectory from molecular mechanism to tumor type specific roles, this review presents a paradigm shift by organizing the regulatory network of SUMOylation in cancer around three pathological axes aberrant cell death, metabolic reprogramming, and immune dysfunction, a framework that aligns more closely with the core pathological drivers of tumor progression and transcends conventional classifications based on tumor type or individual signaling pathways. In parallel, the review emphasizes key nodes of crosstalk with ubiquitination and identifies translational bottlenecks, offering targeted insights for the development of personalized therapeutic strategies directed at the SUMO pathway while establishing a theoretical foundation for SUMOylation as a novel therapeutic axis in oncology.

Reactive nitrogen species (RNS) play a pivotal role in tumorigenesis through complex regulatory networks within the tumor microenvironment (TME). This review summarizes recent advances in understanding RNS-mediated mechanisms, focusing on core components and their concentration-dependent bidirectional effects on tumor cell proliferation, apoptosis, invasion, and metabolism. It explores RNS sources in the TME, including autonomous synthesis by tumor cells and secretion by immune cells (e.g., TAMs, TANs), and their modulation of key signaling pathways (e.g., PI3 K/Akt, NF-κB, HIF-1α). Additionally, the review discusses RNS-mediated regulation of immune responses and angiogenesis, highlighting their dual roles in promoting tumor progression and enabling immune evasion. Finally, it outlines potential clinical applications, such as RNS-targeted diagnostic probes and therapeutic strategies (e.g., iNOS inhibitors, NO donors), providing a foundation for precision oncology.