Prostate cancer is a significant global health issue with inflammation emerging as a critical driver of progression. The prostate tumor microenvironment (TME) is comprised of tumor cells, mesenchymal stem cells, immune cells, cancer-associated fibroblasts, adipocytes, and the extracellular matrix. All of these TME components interact via soluble factors, such as growth factors, cytokines, and chemokines. These interactions remodel the TME and drive inflammation and tumor progression. Prolonged inflammation leads to dysregulated activation and infiltration of immune cells in the TME. This process maintains an immunosuppressive environment and facilitates epithelial-to-mesenchymal transition, migration, and invasion. Chronic inflammation causes inflammatory mediators to enter the circulation over time, as evidenced by systemic biomarkers, such as the systemic immune-inflammation index, which links inflammation to disease severity. Interactions between the prostate gland and adipose tissues further exacerbate systemic inflammation. Inflammation in the prostate gland confers resistance to therapy, primes distant metastatic niches, and promotes metastatic spread, resulting in poor clinical outcomes. Therapeutic strategies, such as anti-inflammatory agents and immunotherapies, hold promise in mitigating disease burden. This review explored the immune landscape of systemic inflammation in prostate cancer, discussed the role of the immune landscape in resistance to therapy and metastasis, and offered insights into potential interventions for targeting inflammation to limit prostate cancer burden.

Organoids are three-dimensional stem cell-derived models that offer a more physiologically relevant representation of tumor biology compared to traditional two-dimensional cell cultures or animal models. Organoids preserve the complex tissue architecture and cellular diversity of human cancers, enabling more accurate predictions of tumor growth, metastasis, and drug responses. Integration with microfluidic platforms, such as organ-on-a-chip systems, further enhances the ability to model tumor-environment interactions in real-time. Organoids facilitate in-depth exploration of tumor heterogeneity, molecular mechanisms, and the development of personalized treatment strategies when coupled with multi-omics technologies. Organoids provide a platform for investigating tumor-immune cell interactions, which aid in the design and testing of immune-based therapies and vaccines. Taken together, these features position organoids as a transformative tool in advancing cancer research and precision medicine.

Hepatocellular carcinoma (HCC), a highly aggressive liver cancer, poses a large medical care burden worldwide. The prognosis of patients with HCC is poor, owing to recurrence and metastasis after common treatment methods. Therefore, identifying new targets to eliminate HCC cells is critical for treatment of HCC without recurrence. PANoptosis, a novel inflammatory cell death pathway, has become an intensively investigated area in recent years. The concept of PANoptosis has brought new hope for HCC therapy, given recent evidence implicating this form of programmed cell death in cancer progression, prognosis, and resistance to chemotherapy and immunotherapy. Despite increasing reviews describing the role of PANoptosis in various cancer types, to our knowledge, no systematic review has examined the implications of PANoptosis in HCC. Therefore, we sought to provide the first systematic review of the regulatory mechanisms and therapeutic potential of PANoptosis in HCC. We summarize recent progress in exploration of the role of PANoptosis in HCC, particularly regulation of the HCC tumor microenvironment by PANoptosis. Finally, we highlight the potential of PANoptosis-based diagnostic and therapeutic strategies for HCC.