Prostate cancer is one of the more heterogeneous tumour types. In recent years, with the rapid development of single-cell sequencing and spatial transcriptome technologies, researchers have gained a more intuitive and comprehensive understanding of the heterogeneity of prostate cancer. Tumour-associated epithelial cells; cancer-associated fibroblasts; the complexity of the immune microenvironment, and the heterogeneity of the spatial distribution of tumour cells and other cancer-promoting molecules play a crucial role in the growth, invasion, and metastasis of prostate cancer. Single-cell multi-omics biotechnology, especially single-cell transcriptome sequencing, reveals the expression level of single cells with higher resolution and finely dissects the molecular characteristics of different tumour cells. We reviewed the recent literature on prostate cancer cells, focusing on single-cell RNA sequencing. And we analysed the heterogeneity and spatial distribution differences of different tumour cell types. We discussed the impact of novel single-cell omics technologies, such as rich omics exploration strategies, multi-omics joint analysis modes, and deep learning models, on future prostate cancer research. In this review, we have constructed a comprehensive catalogue of single-cell omics studies in prostate cancer. This article aimed to provide a more thorough understanding of the diagnosis and treatment of prostate cancer. We summarised and proposed several key issues and directions on applying single-cell multi-omics and spatial transcriptomics to understand the heterogeneity of prostate cancer. Finally, we discussed single-cell omics trends and future directions in prostate cancer.

Hepatocellular carcinoma (HCC), one of the leading causes of cancer‑related mortality worldwide, is challenging to identify in its early stages and prone to metastasis, and the prognosis of patients with this disease is poor. Treatment options for HCC are limited, with even radical treatments being associated with a risk of recurrence or transformation in the short term. Furthermore, the multi‑tyrosine kinase inhibitors approved for first‑line therapy have marked drawbacks, including drug resistance and side effects. The rise and breakthrough of immune checkpoint inhibitors (ICIs) have provided a novel direction for HCC immunotherapy but these have the drawback of low response rates. Since avoiding apoptosis is a universal feature of cancer, the induction of non‑apoptotic regulatory cell death (NARCD) is a novel strategy for HCC immunotherapy. At present, NARCD pathways, including ferroptosis, pyroptosis and necroptosis, are novel potential forms of immunogenic cell death, which have synergistic effects with antitumor immunity, transforming immune ‘cold’ tumors into immune ‘hot’ tumors and exerting antitumor effects. Therefore, these pathways may be targeted as a novel treatment strategy for HCC. In the present review, the roles of ferroptosis, pyroptosis and necroptosis in antitumor immunity in HCC are discussed, and the relevant targets and signaling pathways, and the current status of combined therapy with ICIs are summarized. The prospects of targeting ferroptosis, pyroptosis and necroptosis in HCC immunotherapy are also considered.

Since the theory of modern anatomical partitioning of the prostate was proposed, the differences in the incidence and pathological parameters of prostate cancer between the peripheral zone and transition zone have been gradually revealed. It suggests that there are differences in the pathogenic pathways and molecular biology of prostate cancer between different regions of origin. Over the past decade, advances in sequencing technologies have revealed more about molecules, genomes, and cell types specific to the peripheral and transitional zones. In recent years, the innovation of spatial imaging and multiple-parameter magnetic resonance imaging has provided new technical support for the zonal study of prostate cancer. In this work, we reviewed all the research results and the latest research progress in the study of prostate cancer in the past two decades. We summarized and proposed several vital issues and focused directions for understanding the differences between peripheral and transitional zones in prostate cancer.

Objective: Emerging evidence suggests alterations in gut microbiota (GM) composition following thyroid nodules (TNs) development, yet the causal relationship remains unclear. Utilizing Mendelian Randomization (MR), this study aims to elucidate the causal dynamics between GM and TNs.Methods: Employing summary statistics from the MiBioGen consortium (n=18,340) and FinnGen consortium (1,634 TNs cases, 263,704 controls), we conducted univariable and multivariable MR analyses to explore the GM-TNs association. Techniques including inverse variance weighted, MR-Egger regression, weighted median, and MR-PRESSO were utilized for causal inference. Instrumental variable heterogeneity was assessed through Cochran’s Q statistic and leave-one-out analysis. Reverse MR was applied for taxa showing significant forward MR associations, with multivariate adjustments for confounders.Results: Our findings suggest that certain microbiota, identified as Ruminococcaceae_NK4A214_group (OR, 1.89; 95%CI, 0.47-7.64; p = 0.040), Senegalimassilia (OR, 1.72; 95%CI, 1.03-2.87; p =0.037), Lachnospiraceae (OR,0.64; 95%CI,0.41-0.99; p =0.045), exhibit a protective influence against TNs’ development, indicated by negative causal associations. In contrast, microbiota categorized as Desulfovibrionales (OR, 0.63; 95%CI, 0.41-0.95; p =0.028), Prevotella_7 (OR, 0.79; 95%CI, 0.63-1.00; p =0.049), Faecalibacterium (OR, 0.66; 95%CI, 0.44-1.00; p =0.050), Desulfovibrionaceae (OR, 0.55; 95%CI, 0.35-0.86; p =0.008), Deltaproteobacteria (OR, 0.65; 95%CI, 0.43-0.97; p =0.036) are have a positive correlation with with TNs, suggesting they may serve as risk factors. Reverse MR analyses did not establish significant causal links. After comprehensive adjustment for confounders, taxa Desulfovibrionales (Order), Desulfovibrionaceae (Family), Deltaproteobacteria (Class) remain implicated as potential contributors to TNs’ risk.Discussion: This study substantiates a significant causal link between GM composition and TNs development, underscoring the thyroid-gut axis’s relevance. The findings advocate for the integration of GM profiles in TNs’ prevention and management, offering a foundation for future research in this domain.

Background: Inflammation is considered one of the potential etiological factors in the development and progression of benign prostatic hyperplasia (BPH). However, whether inflammation plays a critical role in the onset or progression of BPH remains controversial. Therefore, we conducted this systematic review and meta-analysis to comprehensively evaluate the impact of histological prostatitis on BPH. Methods: We systematically searched cohort and cross-sectional studies published up to April 2025 in PubMed, the Cochrane Library, Embase, and Web of Science. The quality of the included cohort studies was assessed using the Newcastle-Ottawa Scale (NOS), and cross-sectional studies was evaluated with the Joanna Briggs Institute (JBI) checklist. Data were extracted on prostate volume (PV), International Prostate Symptom Score (IPSS), prostate-specific antigen (PSA), maximum urinary flow rate (Qmax), and residual urine volume (RUV). The effect sizes were pooled using the weighted mean difference (WMD) with corresponding 95% confidence intervals (CIs). Results: A total of 11 studies were included, comprising 6 cohort studies and 5 cross-sectional studies, with a combined sample of 3,135 patients. In cross-sectional studies, compared with patients with BPH alone, those with BPH combined with histological prostatitis had an increase of 1.50 ng/mL in PSA level (95% CI: 0.09 to 2.91; I²=91%; P<0.05), an increase of 3.92 points in IPSS score (95% CI: 2.20 to 5.64; I²=28%; P<0.00001), and an increase of 13.78 mL in PV (95% CI: 10.00 to 17.56; I²=0%; P<0.00001). Qmax decreased by 1.56 mL/s (95% CI: −3.44 to 0.32; I²=80%; P=0.10), with no statistically significant difference. In cohort studies, compared with patients with BPH alone, those with BPH combined with histological prostatitis showed an increase of 1.19 ng/mL in PSA level (95% CI: 0.37 to 2.02; I²=28%; P<0.05), an increase of 10.24 mL in PV (95% CI: 0.79 to 19.69; I²=89%; P<0.05), and a decrease of 2.42 mL/s in Qmax (95% CI: −3.44 to −1.40; I²=65%; P<0.00001). Changes in IPSS (95% CI: −1.33 to 6.22; I²=97%; P=0.20) and RUV (95% CI: −1.66 to 18.07; I²=39%; P=0.10) were not statistically significant. Conclusions: Histological prostatitis may play a promoting role in the progression of BPH. Compared to patients with BPH alone, those with coexisting histological prostatitis exhibited higher PSA levels, higher IPSS, larger PV, and lower Qmax. Therefore, the clinical significance of histological prostatitis should not be overlooked, and it ought to be considered as an important factor in the clinical management of urological patients. Future large-scale prospective studies are warranted to clarify its role in the pathogenesis of BPH.