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| http://dx.doi.org/10.1002/mco2.394 | DOI Listing |
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Immunohistochemical Expression of PD-L1 and CTLA-4 in Triple Negative Breast Cancer and Their Prognostic Associations.
Asian Pac J Cancer Prev
January 2025
Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Objective: Programmed Death-Ligand 1 (PD-L1) and Cytotoxic T Lymphocyte -Associated Antigen-4 (CTLA-4) are presently considered as prognostic markers and therapeutic targets in numerous human malignancies. The goal of this study was to determine whether PD-L1 and CTLA-4 might be used to predict patients' survival in Triple Negative Breast Cancer (TNBC).
Methods: This retrospective cohort study analyzed 100 primary TNBC cases that had surgical resection at the Oncology Center of Mansoura University (OCMU), Faculty of Medicine, Egypt.
CIDEC/FSP27 exacerbates obesity-related abdominal aortic aneurysm by promoting perivascular adipose tissue inflammation.
Life Metab
February 2025
Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200438, China.
Abdominal aortic aneurysm (AAA) is strongly correlated with obesity, partially due to the abnormal expansion of abdominal perivascular adipose tissue (PVAT). Cell death-inducing DNA fragmentation factor-like effector C (CIDEC), also known as fat-specific protein 27 (FSP27) in rodents, is specifically expressed in adipose tissue where it mediates lipid droplet fusion and adipose tissue expansion. Whether and how CIDEC/FSP27 plays a role in AAA pathology remains elusive.
View Article and Find Full Text PDFPreclinical evaluation and preliminary clinical study of Ga-NODAGA-NM-01 for PET imaging of PD-L1 expression.
Cancer Imaging
January 2025
Department of Nuclear Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Hongkou District, No. 100, Haining Road, Shanghai, 200080, China.
Background: Programmed cell death 1/programmed death ligand-1 (PD-L1)-based immune checkpoint blockade is an effective treatment approach for non-small-cell lung cancer (NSCLC). However, immunohistochemistry does not accurately or dynamically reflect PD-L1 expression owing to its spatiotemporal heterogeneity. Herein, we assessed the feasibility of using a Ga-labeled anti-PD-L1 nanobody, Ga-NODAGA-NM-01, for PET imaging of PD-L1.
View Article and Find Full Text PDFPlatinum drugs upregulate CXCR4 and PD-L1 expression via ROS-dependent pathways, with implications for novel combined treatment in gastric cancer.
J Pathol Clin Res
January 2025
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, PR China.
CXC chemokine receptor 4 (CXCR4) and programmed cell death-ligand 1 (PD-L1) are two critical molecules involved in the tumor immune microenvironment. However, the impact of platinum drugs, such as cisplatin, on CXCR4 or PD-L1 expression and the underlying mechanisms in gastric cancer (GC) remain unknown. Moreover, the correlation between their expression levels in GC remains elusive.
View Article and Find Full Text PDFFacile integration of a binary nano-prodrug with αPD-L1 as a translatable technology for potent immunotherapy of TNBC.
Acta Biomater
January 2025
Hengyang Medical School, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, School of Pharmaceutical Science, MOE Key Lab of Rare Pediatric Disease, University of South China, Hengyang 421001, China. Electronic address:
Immune checkpoint blockers (ICBs)-based immunotherapy is a favorable approach for efficient triple-negative breast cancer (TNBC) treatment. However, the therapeutic efficacy of ICBs is greatly compromised by immunosuppressive tumor microenvironments (TMEs) and low expression levels of programmed cell death ligand-1 (PD-L1). Herein, we constructed an amphiphilic prodrug by linking a hydrophobic STING agonist, MSA-2 and a hydrophilic chemotherapeutic drug, gemcitabine (GEM) via an ester bond, which can self-assemble into GEM-MSA-2 (G-M) nanoparticles (NPs) with a tumor growth inhibition (TGI) value of 87.
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