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A portion of gastric cancer patients with negative lymph node metastasis at an early stage eventually die from tumor recurrence or advanced metastasis. Occult lymph node metastasis (OLNM] is a potential risk factor for the recurrence and metastasis in these patients, and it is highly important for clinical prognosis. Positron emission tomography (PET)/computed tomography (CT) is used to assess lymph node metastasis in gastric cancer due to its advantages in anatomical and functional imaging and non-invasive nature. Among the major metabolic parameters of PET, the maximum standardized uptake value (SUVmax) is commonly used for examining lymph node status. However, SUVmax is susceptible to interference by a variety of factors. In recent years, the exploration of new PET metabolic parameters, new PET imaging agents and radiomics, has become an active research topic. This paper aims to explore the feasibility and predict the effectiveness of using PET/CT to detect OLNM. The current landscape and future trends of primary metabolic parameters and new imaging agents of PET are reviewed. For gastric cancer patients, the possibility to detect OLNM non-invasively will help guide surgeons to choose the appropriate lymph node dissection area, thereby reducing unnecessary dissections and providing more reasonable, personalized and comprehensive treatments. [ABSTRACT FROM AUTHOR]

Tumor cells primarily employ the PD-1/PD-L1 pathway to thwart the anti-tumor capabilities of T lymphocytes, inducing immunosuppression. This occurs through the direct interaction of PD-L1 with PD-1 on T lymphocyte surfaces. Recent research focusing on the tumor microenvironment has illuminated the pivotal role of immune cells, particularly tumor-associated macrophages (TAMs), in facilitating PD-L1-mediated immunosuppression. Exosomes, characterized by their ability to convey information and be engulfed by cells, significantly contribute to promoting TAM involvement in establishing PD-L1-mediated immunosuppression within the tumor microenvironment. Exosomes, characterized by their ability to convey information and be engulfed by cells, significantly contribute to promoting TAM involvement in establishing PD-L1-mediated immunosuppression within the tumor microenvironment. In addition to receiving signals from tumor-derived exosomes that promote PD-L1 expression, TAMs also exert control over PD-L1 expression in tumor cells through the release of exosomes. This paper aims to summarize the mechanisms by which exosomes participate in this process, identify crucial factors that influence these mechanisms, and explore innovative strategies for inhibiting or reversing the tumor-promoting effects of TAMs by targeting exosomes. [ABSTRACT FROM AUTHOR]