AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
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Vaccines that use messenger RNA (mRNA) have become a promising platform that is transforming cancer immunotherapy. These mRNA vaccines can be generated and manufactured quickly due to their modular design and can also induce CD4⁺ T-cell and CD8⁺ T-cell responses, in contrast to conventional protein or peptide-based vaccines. Additionally, synthetic mRNA can be optimized through various strategies (e.g., codon optimization, chemical modifications, and polyepitopic design) to not only ensure efficient antigen expression and immune activation but also to mitigate excessive innate immune sensing. Technologies that deliver mRNA vaccines (lipid nanoparticles, dendritic cell-based formulations, self-adjuvanted mRNA constructs, and viral vector systems) have all supported the development of mRNA-vaccine clinical applications while providing unique advantages in stability, antigen presentation, or immunogenicity. Clinical trials in the early phases involving a variety of solid tumors, such as pancreatic cancer, glioblastoma, renal cell carcinoma, melanoma, and non-small cell lung cancer, show that mRNA vaccines can elicit durable T-cell responses, expand high-avidity T-cell clones, and, in some cases, prolong recurrence-free survival. However, the clinical benefit has been variable, often limited by tumor heterogeneity, immune evasion, and immunodominance. Combination strategies utilizing immune checkpoint inhibitors, chemotherapy, and adoptive T-cell therapy are under investigation. This review synthesizes evidence from published clinical studies and 65 registered clinical trials on mRNA-based cancer vaccines, summarizing key molecular principles, delivery strategies, clinical translation in solid tumors, and ongoing opportunities for future therapeutic development.
Gastric cancer (GC) remains a leading cause of cancer-related mortality, with chemoresistance posing a critical barrier to effective treatment. Tumor-associated macrophages (TAMs), particularly the immunosuppressive M2-polarized subset, are emerging as pivotal mediators of chemoresistance within the tumor microenvironment (TME). TAMs promote resistance through multifaceted mechanisms, including activation of pro-survival signaling pathways, induction of epithelial-mesenchymal transition (EMT), and enhancement of angiogenesis. For instance, M2-like TAMs secrete CXCL5, which activates the PI3K/AKT/mTOR axis in GC cells, thereby conferring resistance to 5-fluorouracil (5-FU). Similarly, TMEM, a transmembrane protein overexpressed in cisplatin-resistant GC, drives M2 polarization of TAMs via the Wnt/β-catenin pathway, further amplifying drug resistance and tumor progression. Clinical studies reveal that high TAM infiltration correlates with poor chemotherapy response and reduced survival in GC patients. This review synthesizes current evidence on TAM-driven chemoresistance in GC, highlighting the molecular interplay between TAMs, tumor cells, and stromal components. It underscores the potential of TAM-centric therapies-including checkpoint inhibitors, epigenetic modulators, and combination regimens-to overcome resistance and improve clinical outcomes. By integrating preclinical insights and clinical data, this work provides a roadmap for developing precision therapies that exploit TAM biology to enhance chemosensitivity in GC.
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