Immune checkpoint blockade (ICB) therapy has been successfully applied to clinically therapeutics in multiple cancers, but its efficacy varies greatly among different patients and cancer types. Therefore, the construction of gene signatures to identify patients who could benefit from ICB therapy is particularly important for precision cancer treatment. However, due to the lack of a user-friendly platform, the construction of such gene signatures is a great challenge for clinical investigators who have limited programming skills. In light of this challenge, we developed a web server called Tumor Immunotherapy Response Signature Finder(TIRSF) for the construction of gene signatures to predict ICB therapy response in cancer patients. TIRSF consists of three functional modules. The first module is the Signature Discovery module which provides signature construction and performance evaluation functionalities. The second is a module for response prediction based on the TIRSF signatures, which enables response prediction and prognostic analysis of immunotherapy samples. The last is a module for response prediction based on existing signatures. This module currently integrates 24 published signatures for ICB therapy response prediction. Together, all of above features can be freely accessed at http://tirsf.renlab.org/.
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http://dx.doi.org/10.1093/nar/gkac374 | DOI Listing |
Over the last decade, Hippo signaling has emerged as a major tumor-suppressing pathway. Its dysregulation is associated with abnormal expression of and -family genes. Recent works have highlighted the role of YAP1/TEAD activity in several cancers and its potential therapeutic implications.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Department of Pharmacology, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, People's Republic of China.
Background: Chronic kidney disease (CKD) is a progressive condition that arises from diverse etiological factors, resulting in structural alterations and functional impairment of the kidneys. We aimed to establish the Anoikis-related gene signature in CKD by bioinformatics analysis.
Methods: We retrieved 3 datasets from the Gene Expression Omnibus (GEO) database to obtain differentially expressed genes (DEGs), followed by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, Gene Set Enrichment Analysis (GSEA) and Gene Set Variation Analysis (GSVA) of them, which were intersected with Anoikis-related genes (ARGs) to derive Anoikis-related differentially expressed genes (ARDEGs).
Front Immunol
January 2025
Key Lab of Cell Differentiation and Apoptosis of Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Introduction: Breast cancer (BC) is the most prevalent malignant tumor in women, with triple-negative breast cancer (TNBC) showing the poorest prognosis among all subtypes. Glycosylation is increasingly recognized as a critical biomarker in the tumor microenvironment, particularly in BC. However, the glycosylation-related genes associated with TNBC have not yet been defined.
View Article and Find Full Text PDFFront Immunol
January 2025
Division of Allergy, Immunology and Rheumatology, University of Rochester Medical Center, Rochester, NY, United States.
While durable antibody responses from long-lived plasma cell (LLPC) populations are important for protection against pathogens, LLPC may be harmful if they produce antibodies against self-proteins or self-nuclear antigens as occurs in autoimmune diseases such as systemic lupus erythematosus (SLE). Thus, the elimination of autoreactive LLPC may improve the treatment of antibody-driven autoimmune diseases. However, LLPC remain a challenging therapeutic target.
View Article and Find Full Text PDFFront Immunol
January 2025
Division of Urology, Department of Surgery, Endeavor Health (formerly NorthShore University HealthSystem), Evanston, IL, United States.
Introduction: Macrophages exhibit marked phenotypic heterogeneity within and across disease states, with lipid metabolic reprogramming contributing to macrophage activation and heterogeneity. Chronic inflammation has been observed in human benign prostatic hyperplasia (BPH) tissues, however macrophage activation states and their contributions to this hyperplastic disease have not been defined. We postulated that a shift in macrophage phenotypes with increasing prostate size could involve metabolic alterations resulting in prostatic epithelial or stromal hyperplasia.
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