Given the high malignancy of liver cancer and the liver’s unique role in immune and metabolic regulation, current treatments have limited efficacy, resulting in a poor prognosis. Hydrogels, soft 3-dimensional network materials comprising numerous hydrophilic monomers, have considerable potential as intelligent drug delivery systems for liver cancer treatment. The advantages of hydrogels include their versatile delivery modalities, precision targeting, intelligent stimulus response, controlled drug release, high drug loading capacity, excellent slow-release capabilities, and substantial potential as carriers of bioactive molecules. This review presents an in-depth examination of hydrogel-assisted advanced therapies for hepatocellular carcinoma, encompassing small-molecule drug therapy, immunotherapy, gene therapy, and the utilization of other biologics. Furthermore, it examines the integration of hydrogels with conventional liver cancer therapies, including radiation, interventional therapy, and ultrasound. This review provides a comprehensive overview of the numerous advantages of hydrogels and their potential to enhance therapeutic efficacy, targeting, and drug delivery safety. In conclusion, this review addresses the clinical implementation of hydrogels in liver cancer therapy and future challenges and design principles for hydrogel-based systems, and proposes novel research directions and strategies.

Background: A number of studies have attempted to determine the prognostic significance of proliferating cell nuclear antigen (PCNA) in patients with colorectal cancer (CRC), but the reports are controversial and inconsistent. Thus, we conducted a meta-analysis to clarify the value of PCNA in CRC prognosis. Methods: A systematic search of relevant studies was performed in 4 electronic databases including PubMed, Cochrane Library, Embase, and Web of Science until February 2018. Hazard ratios (HRs) combined with 95% confidence intervals (95% CIs) were used to evaluate the relationship of PCNA expression with overall survival (OS), cancer-specific survival (CSS), and disease-free survival (DFS). Results: A total of 1372 CRC patients in 14 studies were identified eventually in our meta-analysis. The pooled HRs demonstrated that CRC patients with high PCNA expression was significantly correlated with poor OS (HR = 1.81; 95% CI: 1.51–2.17; P = .000), CSS (HR = 1.99; 95% CI: 1.04–3.79; P = .037); but not significantly with DFS (HR = 2.48; 95% CI: 0.98–6.26; P = .055). Sensitivity analysis showed the pooled HRs for OS, CSS, and DFS were stable when the included studies were removed one by one. Conclusion: Our meta-analysis suggested that high PCNA expression was associated with poor prognosis, and it could serve as a reliable and prognostic biomarker in CRC patients. More large-scale studies are needed to further support the conclusion.

We aimed to compare the overall survival (OS) and standardized mortality rate (SMR) of the male breast cancer (MBC) with female breast cancer (FBC) after propensity score matching. Based on the Surveillance, Epidemiology, and End Results (SEER), the early breast cancer patients (T_1–2N_0–2M₀) were extracted from 1998–2007. This study included 1,111 and 2,151 patients with early MBC and FBC, respectively, whose clinicopathological characteristics were well balanced. At a mean follow-up time of 97 months, 10-year OS rate was 58.3% in the MBC group and 68.7% in the FBC (log-rank test, P < 0.001; hazard ratio (HR) = 1.45, 95% confidence interval (CI) = 1.29 to 1.64). Adjusted HR for OS between MBC and FBC were revealed from propensity score matched-multivariable Cox proportional hazards models (HR = 1.53, 95% CI = 1.35 to 1.73). Similar adjusted SMRs between MBC and FBC ((SMR = 1.98, 95% CI = 1.83,2.14) for FBC and (SMR = 2.07, 95% CI = 1.88–2.28) for MBC) were observed. The nomogram was constructed for FBC, and predicted probabilities were generally good (C-index = 0.71), whose area under curve is higher than TNM stage classification (0.74 vs 0.62). OS was significantly decreased among early MBC patients compared with FBC, but similar SMRs and its trends by age groups were observed between MBC and FBC except for young patients.

Pancreatic ductal adenocarcinoma (PDAC), the predominant subtype of pancreatic cancer, ranks among the deadliest malignancies worldwide, with a 5-year survival rate remaining below 13 %. Its poor prognosis stems from complex anatomical barriers, a dense and heterogeneous tumor microenvironment (TME), and intricate molecular regulatory networks that collectively hinder early detection and limit therapeutic efficacy. Nanomedicine offers promising solutions by enhancing drug loading, improving delivery, counteracting drug resistance, and enabling stimuli-responsive control. Notably, stimuli-responsive nanotherapeutics have emerged as a transformative strategy, achieving precise drug release through activation by endogenous TME cues (e.g., acidic pH, redox gradients, hypoxia, enzyme overexpression) or exogenous triggers (e.g., ultrasound, light, magnetic fields). Endogenous-responsive systems autonomously activate at tumor sites, enhancing intratumoral drug accumulation and reducing off-target effects, while exogenous-responsive platforms enable spatiotemporal control through external modulation. Multi-responsive systems integrate both mechanisms to achieve dynamic and synergistic therapeutic effects, holding significant promise for PDAC theranostics. This review summarizes recent advances in stimuli-responsive nanotherapeutics for PDAC, detailing their activation mechanisms, biomedical applications, and theranostic potential across endogenous, exogenous, and multi-responsive modalities. It further discusses current challenges and future directions for translating these technologies into clinical practice.

Sonodynamic therapy (SDT) exhibits clinical potential for deep-tissue tumor treatment due to its deep tissue penetration and spatiotemporal controllability. Its core mechanism relies on ultrasound-activated sonosensitizers to generate reactive oxygen species (ROS), thereby inducing tumor cell apoptosis. However, conventional sonosensitizers face limitations in ROS yield and tumor-targeting efficiency. In this study, we innovatively designed a multifunctional metal–organic nanosheet (TiZrRu-MON) by hydrothermal coordination of [Ru(bpy)₃]2⁺ photosensitizing units with TiZr-O clusters, while incorporating Fe3⁺ to construct a cascade catalytic system. Experimental results demonstrated that: (1) Fe3⁺ lattice doping significantly enhanced charge carrier mobility and ultrasound-triggered 1O₂ quantum yield via the formation charge transfer channels; (2) The acidic tumor microenvironment activated Fe3⁺-mediated Fenton reactions, establishing a positive feedback loop with SDT to synergistically amplify ROS generation; (3) Hyaluronic acid functionalization improved nanosheet internalization in HepG2 tumor cells through CD44 receptor-mediated endocytosis. Remarkably, ultrasound irradiation induced substantial oxidative stress and immunogenic cell death, promoting the release of damage-associated molecular patterns (DAMPs), which elevated the maturation rate of tumor-infiltrating dendritic cells (DCs) and significantly increased the proportion of CD8⁺ T cells. In a mouse subcutaneous tumor model, the system achieved effective tumor suppression with manageable systemic toxicity. This work proposes a metal–ligand coordination strategy to advance the development of high-performance sonosensitizers and immunomodulatory antitumor technologies.

Background: The peroxiredoxin family, a crucial regulator of redox reactions, is strongly associated with various tumorigenesis. However, the role of peroxiredoxin4 (PRDX4) in colon adenocarcinoma (COAD) remains poorly understood.Methods: Multicenter databases, including GEPIA, HPA, UALCAN, cBioPortal, cancerSEA, STRING, CCLE, and LinkedOmics, comprehensively analyzed transcriptional expression, prognostic value, genetic alterations, signaling pathways, and associated genes of the PRDXs in COAD patients. Colony formation, transwell, flow cytometry, sphere formation, and xenograft assays were performed to validate further in vitro and in vivo.Results: Members of the PRDX family were differentially expressed in COAD, with each member showing varying degrees of genetic alterations. Intriguingly, only PRDX4 significantly correlated with COAD prognosis and stage. The single-cell sequencing suggested that PRDX4 is positively correlated with proliferation, apoptosis, and invasion, whereas negatively correlated with stemness. Moreover, PRDX4 involved in a series of critical biological processes, such as cell growth. Furthermore, in vivo and in vitro analyses indicated that knocking down PRDX4 inhibits the proliferation and invasion of HCT116 cells while promoting apoptosis and stemness.Conclusions: We identified PRDX4 expression as a novel potential prognostic marker in COAD.