β2-Microglobulin (β2m) is essential for the stability and surface expression of human leukocyte antigen class I (HLA-I) molecules. While β2m's structural role is well established, its influence on the antigenic landscape remains incompletely understood. Here, we investigated how constitutive β2m binding to HLA-I influences the antigenic landscape in the context of cancer-associated epitopes. Using two engineered cell lines expressing β2m fused to the HLA-I heavy chain, we analysed changes in immunopeptidomes and epitope presentation. Despite cell line-specific transcriptional responses, the fusion of β2m to HLA-I consistently reduced peptide editing and resulted in convergent remodelling of the antigen presentation pathway (APP). The fusion further altered peptide selection, favouring the display of lower-affinity peptides derived from endogenous proteins while impairing high-affinity peptide presentation on HLA-I molecules. These changes were not attributable to APP component abundance but rather reflected mechanistic alterations in peptide selection and impacted T cell receptor recognition of tumour epitopes. Our findings suggest that β2m-HLA-I fusion can distort the physiological antigenic repertoire and T cell recognition, with implications for epitope discovery, immunotherapy design, and studies of HLA-I-mediated immune surveillance.

Pulsed electric field (PEF) ablation is a promising nonthermal tumor treatment for liver cancer, recognized for its ability to induce immune responses. However, the field has lacked a comprehensive bibliometric evaluation. This study aimed to provide an in-depth analysis of the research landscape.

In total, 691 English-language articles on PEF-based liver cancer therapy, published between 1989 and 2025, were identified from the Scopus and Web of Science databases. Bibliometric tools, including VOSviewer, CiteSpace, Scimago Graphica, and Bibliometrix, were applied to perform coauthorship, cocitation, and keyword cooccurrence analyses, focusing on contributions from countries, institutions, authors, and journals.

Research on PEF therapy in liver cancer has grown steadily, showing an annual increase of 9.7%. The United States and China were the most influential contributors, with the former leading in both total publications and citations. Major contributing institutions included Zhejiang University, Zhongshan University, and Northwestern University, with Leen Edward, Nuccitelli Richard, and Davalos Rafael V. the most frequently cocited authors. Journal of Vascular and Interventional Radiology was the most productive journal in the field. Radiology showed the highest total link strength in cocitation analysis. Co-occurrence analyses of keywords and cocited references highlighted the tumor microenvironment and immunotherapy as emerging research priorities.

PEF therapy for liver cancer is advancing rapidly and holds strong clinical promise. Future research will likely focus on the tumor microenvironment, immune mechanisms, and field parameter optimization. Strengthened international collaboration is essential to foster innovation and expand clinical applications.

Targeted protein degradation (TPD) has emerged as a promising therapeutic strategy to address cancer drug resistance by enabling the selective and efficient degradation of disease-associated proteins through cellular mechanisms. Since 2020, lysosome-targeting chimeras (LYTACs) have gained attention for expanding targeted protein degradation to extracellular and membrane-associated disease-related proteins beyond the reach of proteolysis-targeting chimeras (PROTACs). In practice, LYTACs can overcome resistance by degrading instead of inhibiting them. This efficient and durable removal of resistance-associated drivers thereby suppresses compensatory signaling, restores drug sensitivity, and contributes to remodeling the tumor microenvironment. To facilitate the clinical translation of this emerging technology, this review systematically compares the mechanistic and functional advantages of LYTACs over PROTACs, summarizes key design principles, and categorizes major LYTAC modalities, including AbTACs, MoDE-As, and nano-LYTACs. We further discuss their in vivo pharmacological behaviors, with particular emphasis on stability, tumor selectivity, and degradation efficiency. Importantly, this article comprehensively highlights recent advances in the application of LYTACs for overcoming therapeutic resistance, including resistance to chemotherapy, targeted therapy, and immunotherapy. Finally, current translational bottlenecks, such as delivery efficiency, receptor heterogeneity, and pharmacokinetic limitations, are critically analyzed. Collectively, while still in its early stages of development, LYTAC-based lysosomal degradation represents a promising, paradigm-shifting strategy for targeting previously intractable mechanisms of cancer resistance.

Urachal anomalies are rare entities in the adult population with significant malignant potential. This study aims to comprehensively describe clinical and paraclinical characteristics, as well as to analyze and evaluate prognostic factors for urachal carcinoma, thereby facilitating early diagnosis and effective management.

We conducted a retrospective study on patients diagnosed with urachal anomalies from 2017 to 2025. Data regarding clinical characteristics, imaging findings, treatment modalities, and clinical outcomes were collected for both benign and malignant cases. Additionally, survival outcomes were specifically analyzed for patients with urachal carcinoma.

A total of 112 patients were included, comprising 8.9% cases of urachal carcinoma, while infection was the predominant presentation (72.3%). Surgical management differed significantly by pathology, with urachal excision and partial cystectomy performed in 80.0% of malignant cases versus 23.9% of benign cases. Multivariate logistic regression identified hematuria (Odds Ratio (OR) 14.1; 95% Confidence Interval (CI) 1.3-153.6; p = 0.03) and calcification (OR 13.5; 95% CI 1.7-109.2; p = 0.01) as significant independent predictors of malignancy. Histologically, adenocarcinoma was the major subtype (80%), with most tumors being Sheldon stage IIIA or IV. Overall survival (OS) showed a steep decline, recorded at 90.0%, 60.0%, and 15.0% at 1, 3, and 5 years, respectively.

Gross hematuria and calcification serve as critical, independent predictors of urachal malignancy. Given the aggressive nature and poor overall prognosis (5-year OS of only 15.0%), the presence of these indicators necessitates an aggressive diagnostic workup and prompt radical surgical intervention (en-bloc urachal excision with partial cystectomy) to optimize long-term patient outcomes.

Spiritual distress represents a significant yet under-addressed dimension of suffering among children with cancer. Despite its influence on emotional resilience, treatment adherence, and psychological well-being, spiritual care in pediatric oncology remains inconsistently implemented due to developmental misalignment, cultural variability, and limited professional training.

This study aimed to synthesize the literature and propose a a preliminary, developmentally responsive, and culturally adaptable nursing-centered conceptual framework for spiritual care in pediatric oncology, designed to guide nursing practice while supporting interdisciplinary collaboration in pediatric oncology, termed the Developmental-Spiritual Oncology Care Model (DSOCM).

An integrative literature review was conducted across six databases, yielding 227 sources, including empirical studies, theoretical works, clinical guidelines, and foundational texts. A manual inductive thematic analysis was performed to identify recurring concepts, relational patterns, and care processes relevant to pediatric spiritual care. Selected theoretical foundations-including Fowler's Faith Development Theory, Watson's Caring Theory, Travelbee's Human-to-Human Relationship Model, Benner's Competency Framework, and Mercer's spiritual constructs- were critically evaluated and used to inform the development of the conceptual framework.

DSOCM proposes core assumptions, paradigmatic and meta-paradigmatic concepts, guiding objectives, and a holistic nursing care approach. The framework highlights inclusivity, interdisciplinary collaboration, and competency-based training.

As a preliminary literature-derived conceptual framework, DSOCM offers a structured guide for spiritual nursing care in pediatric oncology and requires further empirical testing, cross-cultural adaptation, and contextual refinement.

Colorectal cancer, a major health issue worldwide, exhibits intricate molecular mechanisms that necessitate further exploration, particularly regarding regulated cell death pathways, such as ferroptosis. This study investigated the role of the immunophilin FKBP9 (FK506 Binding Protein 9) in colon cancer, specifically its effects on cell proliferation and ferroptosis resistance. Using molecular biology techniques, including quantitative reverse transcription PCR, Western blotting, and cell proliferation assays, we established that FKBP9 is overexpressed in colon cancer cell lines HCT116 and SW480. Furthermore, we demonstrated that FKBP9 enhances cell proliferation by inhibiting ferroptosis through glutathione peroxidase 4 (GPX4) expression upregulation, thereby reducing reactive oxygen species levels and stabilizing GPX4 by preventing its autophagic degradation. Notably, increased FKBP9 expression is associated with lower overall survival rates in patients with colon cancer, suggesting its potential as a prognostic marker. These findings underscore the therapeutic potential of FKBP9 in colon cancer, offering a new method to sensitize cancer cells to ferroptosis and improve patient outcomes.

Aimed to characterize the clinical and ultrasound characteristics of ovarian Sertoli-Leydig cell tumors (SLCTs) with standardized terminology.

A retrospective analysis was conducted on individuals diagnosed with ovarian SLCTs at West China Second University Hospital between January 2015 and January 2025, and confirmed by pathology and immunohistochemistry. The International Ovarian Tumor Analysis (IOTA) terminology was employed to systematically describe the sonographic features of ovarian SLCTs. The study compiled the clinical and sonographic characteristics of ovarian SLCTs, drawing from cases at WCSUH-SCU and a literature review performed utilizing PubMed from January 1, 1995, to July 31, 2025.

Seventeen subjects, aged 12-77 (median, 32) years, were encompassed in the cohort. Three subjects had well-differentiated tumors, eight had moderately differentiated tumors, and six had poorly differentiated tumors. Fourteen subjects presented with endocrine symptoms. Eleven subjects with well- or moderately-differentiated SLCTs underwent unilateral salpingo-oophorectomy or ovarian tumor resection. Ultrasound examinations revealed that most lesions were regularly round or ovoid (82.4%), had regular margins (94.1%), had uniform echogenicity (58.8%), and were hypoechogenic (88.2%). Most lesions displayed moderate to abundant vascularity (color score of 3-4, 76.5%). A literature retrieval yielded 14 articles reporting the ultrasonographic features of 44 ovarian SLCT cases with characteristics comparable to those in the present cohort.

The ultrasonographic features of ovarian SLCTs include hypoechoic masses with homogeneous or heterogeneous echogenicity, often containing cystic components within the lesions. Scattered vascular distribution is observed within the tumor, with circumferential vascular patterns in some cases, and these lesions are frequently accompanied by endocrine symptoms.

Although most prostate tumors are relatively indolent, advanced disease can progress to aggressive, often lethal variants, including neuroendocrine prostate cancer (NEPC). To identify drivers of aggressive prostate cancer, we used Sleeping Beauty (SB) transposon mutagenesis in a mouse model having prostate-specific loss of Pten and Tp53 (NPp53 mice). Compared with control NPp53-SB(-) mice, experimental NPp53-SB(+) mice developed more aggressive tumors with increased metastasis. Notably, NPp53-SB(+) mice exhibited NEPC phenotypes with transcriptomic features that recapitulate human NEPC. Analysis of recurrent common insertion sites (CIS) and associated genes (CIS genes) identified genes differentially expressed between NEPC and non-NEPC tumors. Analysis of NEPC-enriched CIS genes by cross-species integration of genomic and transcriptomic data prioritized sirtuin 1 (Sirt1) as a candidate mechanistic determinant of NEPC. Gain- and loss-of-function studies in human prostate cancer cells and mouse NEPC organoids confirmed that SIRT1 promotes NEPC, while pharmacological inhibition suppresses it. Thus, integration of cross-species analyses with an unbiased forward genetic screen uncovered novel drivers of NEPC.

BackgroundIntegrated bioinformatics approaches were used to identify stage-specific candidate genes and potential drug targets in triple-negative breast cancer (TNBC).MethodsMicroarray (164 early-stage, 33 advanced-stage, and 53 normal samples) and RNA-seq (113 normal, 163 early-stage, and 30 advanced-stage TNBC samples) datasets were analyzed. Differentially expressed genes (DEGs) were identified, followed by co-expression analysis using Weighted Gene Co-expression Network Analysis (WGCNA) and protein-protein interaction analysis using the STRING database. miRNA co-regulation was evaluated using multiMiR and TCGA correlation analyses. Candidate genes were validated using UALCAN and immunohistochemistry data. Molecular docking assessed potential therapeutic agents.ResultsNovel stage-specific candidate biomarkers were identified, including DNAJC6, SKP2, MOCOS, and NCAPD2 in early-stage TNBC, and F11R, FOXO6, PPP4C, and TMEM51 in advanced-stage TNBC. UALCAN analysis confirmed the dysregulation of these genes across 23 additional malignancies. STRING-based network analysis revealed stage-specific protein-protein interactions, including SKP2-SKP1 in early-stage and F11R-TJP1 in advanced-stage TNBC. miRNA co-regulation distinguished early-stage TNBC through PI3K-AKT-related pathways and advanced-stage TNBC through tumor progression-associated pathways. Docking-based drug repurposing highlighted conventional agents (e.g., doxorubicin) and potential novel candidates (e.g., sunitinib).ConclusionThis study identifies novel stage-specific gene candidates and suggests repurposable drugs for TNBC, supporting progression-specific targeted therapeutic strategies.

Objective To investigate the heterogeneity characteristics of cancer-associated fibroblasts (CAF) in acral melanoma (AM) and their functional roles in the tumor microenvironment (TME), providing a theoretical basis for developing effective therapeutic strategies. Methods The single-cell RNA sequencing data used in this study were previously generated by our research group and have been deposited in the HRA001804 dataset of the National Genomics Data Center (NGDC). Five AM patient samples were selected from this dataset for analysis, including 4 primary tumor samples (PL1, PL2, PL4, PL5) and 1 lymph node metastasis sample (LG2). Bioinformatics methods including unsupervised clustering, pseudotime trajectory analysis, transcription factor regulatory network analysis, and cell-cell communication analysis were used for data mining. Results Three subtypes of CAF were identified from 41 960 high-quality cells: immunomodulatory CAF (iCAF), myofibroblastic CAF (mCAF), and proliferative CAF (pCAF). Pseudotime trajectory analysis demonstrated that mCAF were located at the initiation of differentiation, while iCAF and pCAF were distributed in distinct terminal branches. FOS-like 1, AP-1 transcription factor subunit (FOSL1) was identified as a key transcription factor regulating the differentiation of CAF into pCAF, and its co-expression modules were enriched in the P53 signal pathway, AP-1 transcription factor network, and MYC-mediated cell proliferation pathways. Cell communication analysis revealed an interaction network centered on iCAF, with critical pathways including CSPG4-(ITGA2+ITGB1), GDF15-TGFBR2, LGALS9-CD45/CD44, and CD70-CD27 signal pathways. Conclusion CAF in AM exhibits high heterogeneity, with FOSL1 playing a key regulatory role in CAF differentiation. CAF participates in tumor microenvironment regulation through complex intercellular communication networks. These findings provide important insights into understanding the biological characteristics of acral melanoma and developing targeted therapeutic strategies.