Background: Benign prostatic hyperplasia (BPH) is a common issue among older men. Diagnosis of BPH currently relies on imaging tests and assessment of urinary flow rate due to the absence of definitive diagnostic markers. Developing more accurate markers is crucial to improve BPH diagnosis.Method: The BPH dataset utilized in this study was sourced from the Gene Expression Omnibus (GEO). Initially, differential expression and functional analyses were conducted, followed by the application of multiple machine learning techniques to identify key diagnostic markers. Subsequent investigations have focused on elucidating the functions and mechanisms associated with these markers. The ssGSEA method was employed to evaluate immune cell scores in BPH samples, facilitating the exploration of the relationship between key diagnostic markers and immune cells. Additionally, molecular docking was performed to assess the binding affinity of these key markers to therapeutic drugs for BPH. Tissue samples from BPH patients were collected for experimental validation of the expression differences of the aforementioned genes.Result: A total of 185 differential genes were identified, comprising 67 up-regulated and 118 down-regulated genes. These genes are implicated in pathways that regulate extracellular matrix tissue composition and cellular responses to transforming growth factor beta stimulation, as well as critical signaling pathways such as AMPK and mTOR. Through the application of various machine learning techniques, DACH1, CACNA1D, STARD13, and RUNDC3B were identified as key diagnostic markers. The ssGSEA algorithm further corroborated the association of these diagnostic genes with diverse immune cells. Moreover, molecular docking analysis revealed strong binding affinities of these markers to tamsulosin and finasteride, suggesting their potential as drug targets. Finally, experimental validation confirmed the expression differences of DACH1, CACNA1D, STARD13, and RUNDC3B in BPH tissues.Conclusion: This study introduces novel immune-related diagnostic markers for BPH and highlights their promise as new drug targets, providing a valuable approach for predictive diagnosis and targeted therapy of BPH.

Aberrations in MYC underlie a large proportion of liver hepatocellular carcinoma (LIHC) cases; however, MYC is difficult to target because of its undruggable structure. We aimed to uncover MYC-associated molecular targets to provide new strategies for LIHC treatment. LIHC transcriptome datasets and clinical information were obtained from The Cancer Genome Atlas. A series of bioinformatics analyses were performed for 370 patients who were stratified based on the median MYC expression level (high-MYC group and low-MYC group). Correlation analysis was performed to determine relationships between the expression of key MYC-associated genes and prognosis, DNA promotor methylation, and immune cell infiltration. Gene ontology and Kyoto Encyclopedia of Genes and Genomes Pathway enrichment analyses were performed to elucidate the functions of these genes in LIHC. Their expression and functions in LIHC were further verified using transgenic mice overexpressing c-Myc under control of the hepatocyte-specific promoter (Alb-Cre). AURKB, CCNB2, and CDKN3 were overexpressed in LIHC patients with high MYC expression and were associated with poor prognosis. Upregulation of these 3 genes was significantly correlated with hypomethylated promoter status, advanced T stage, metastasis, and immune cell infiltration in LIHC patients. Functional enrichment analyses indicated that these genes participate in the "p53 signaling pathway" and "cell cycle". Furthermore, RT-PCR and IHC analysis revealed that their mRNA and protein expression levels were upregulated in an Alb-Cre;cMYC^lsl/- mouse model. Drugs that target these 3 MYC-related genes were identified. Taken together, our results identify biomarkers of potential utility for managing liver cancer therapy owing to their significance in tumorigenesis, proliferation, and tumor immunity.

Pancreatic cancer, referred to as the "monarch of malignancies," is a neoplastic growth mostly arising from the epithelial cells of the pancreatic duct and acinar cells. This particular neoplasm has a highly unfavorable prognosis due to its marked malignancy, inconspicuous initial manifestation, challenging early detection, rapid advancement, and limited survival duration. Cellular immunotherapy is the ex vivo culture and expansion of immune effector cells, granting them the capacity to selectively target malignant cells using specialized techniques. Subsequently, these modified cells are reintroduced into the patient's organism with the purpose of eradicating tumor cells and providing therapeutic intervention for cancer. Presently, the primary cellular therapeutic modalities employed in the treatment of pancreatic cancer encompass CAR T-cell therapy, TCR T-cell therapy, NK-cell therapy, and CAR NK-cell therapy. This review provides a concise overview of the mechanisms and primary targets associated with various cell therapies. Additionally, we will explore the prospective outlook of cell therapy in the context of treating pancreatic cancer.

Synthetic lethality is a phenomenon wherein the simultaneous deficiency of two or more genes results in cell death, while the deficiency of any individual gene does not lead to cell death. In recent years, synthetic lethality has emerged as a significant topic in the field of targeted cancer therapy, with certain drugs based on this concept exhibiting promising outcomes in clinical trials. Nevertheless, the presence of tumor heterogeneity and the intricate DNA repair mechanisms pose challenges to the effective implementation of synthetic lethality. This review aims to explore the concepts, development, and ethical quandaries surrounding synthetic lethality. Additionally, it will provide an in-depth analysis of the clinical application and underlying mechanism of synthetic lethality.

DNA damage response (DDR) pathways are essential for maintaining genomic integrity. Accumulating pan-cancer evidence, however, reveals that alterations within these networks act as widespread drivers of tumor initiation, progression, and therapeutic vulnerability. This review synthesizes the biological mechanisms and clinical implications of DDR defects across solid tumors. We first detail how the disruption of major DDR pathways leads to profound genomic instability and characteristic mutational heterogeneity. Building on this mechanistic foundation, we evaluate the interaction between DDR deficiencies and the tumor immune microenvironment to highlight emerging opportunities for immunotherapy. We also critically examine recent advances in targeted treatment paradigms based on synthetic lethality, focusing particularly on the evolving clinical landscape of PARP inhibitors. Finally, we link these biological insights directly to clinical practice by discussing genetic risk assessment, biomarker development, and precision therapeutic decision-making. Ultimately, a deeper understanding of these alterations is essential to develop more effective targeted and combinatorial therapies for patients with DDR-deficient malignancies.

The tumor microenvironment significantly influences the aggressive invasive characteristics of human solid tumors, with the infiltration of immune cells being a defining feature of tumor advancement. Among the diverse cell types present in the tumor microenvironment, tumor-associated macrophages (TAMs) stand out as crucial regulatory centers in the interplay between tumors and the immune system. Recent developments in single-cell sequencing technologies, combined with an expanding body of research, have revealed the functional diversity and heterogeneity of TAMs, as well as the mechanisms through which they interact within the tumor microenvironment. This indicates that TAMs could represent innovative targets for therapies aimed at tumors, thus promoting the creation of tailored anti-cancer strategies. This article provides a review of the various types of TAMs, their influence on tumor development and progression, their regulatory functions in tumor activities, and the progress in tumor immunotherapy that focuses on targeting TAMs.