Tumor immunotherapy has emerged as a formidable strategy, demonstrating substantial achievements in the field of cancer treatment. Despite its remarkable success, intrinsic limitations such as insufficient targeting capabilities, side effects, and resistance to immunotherapy hinder its efficacy. To address these challenges, the utilization of nanomedicines in tumor immunotherapy has been broadly explored, capitalizing on their advantages of targeting delivery capability, loading capacity, modifiability, and biocompatibility. Through rational design approaches, nanomedicines are engineered to meet diverse delivery requirements and synergize with different regimens to maximize therapeutic efficacy while alleviating side effects. This review initially discusses the challenges associated with tumor immunotherapy and underscores the pivotal role played by nanomedicines in overcoming these obstacles. Subsequently, representative types of nanoparticles are systematically introduced based on their structural properties, advantages, potential limitations, and future research directions. Special emphasis is placed on recent advancements in a range of nanomedicines designed for specific tumor immunotherapy strategies. Finally, the clinical applications as well as prospects of nanomedicines are discussed.
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http://dx.doi.org/10.1093/jmcb/mjae055 | DOI Listing |
BI 1703880, a novel STimulator of INterferon Genes (STING) agonist, has demonstrated preclinical antitumor activity. As STING activation can upregulate programmed death ligand 1 and human leukocyte antigen in tumor cells, a combination of BI 1703880 and an anti-programmed cell death protein 1-antibody, such as ezabenlimab, may improve efficacy. This first-in-human phase Ia study (NCT05471856) is evaluating BI 1703880 plus ezabenlimab in patients with advanced solid tumors.
View Article and Find Full Text PDFDiagn Interv Radiol
January 2025
Huadong Hospital, Fudan University, Department of Thoracic Surgery, Shanghai, China.
Purpose: Patients with advanced non-small cell lung cancer (NSCLC) have varying responses to immunotherapy, but there are no reliable, accepted biomarkers to accurately predict its therapeutic efficacy. The present study aimed to construct individualized models through automatic machine learning (autoML) to predict the efficacy of immunotherapy in patients with inoperable advanced NSCLC.
Methods: A total of 63 eligible participants were included and randomized into training and validation groups.
J Cachexia Sarcopenia Muscle
February 2025
Center for Health Information Partnerships, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Background: Cancer-associated cachexia can inhibit immune checkpoint inhibitor (ICI) therapy efficacy. Cachexia's effect on ICI therapy has not been studied in large cohorts of cancer patients aside from lung cancer. We studied associations between real-world routinely collected clinical cachexia markers and disability-free, hospitalization-free and overall survival of cancer patients.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Second Department of Oncology, Guangdong Second Provincial General Hospital, Guangzhou, China.
Background: SET domain-containing protein 4 (SETD4) is a histone methyltransferase that has been shown to modulate cell proliferation, differentiation, and inflammatory responses by regulating histone H4 trimethylation (H4K20me3). Previous reports have demonstrated its function in the quiescence of cancer stem cells as well as drug resistance in several cancers. A limited number of systematic studies have examined SETD4's role in the tumor microenvironment, pathogenesis, prognosis, and therapeutic response.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Biochemistry and Molecular Genetics and.
Mutations or homozygous deletions of MHC class II (MHC-II) genes are commonly found in B cell lymphomas that develop in immune-privileged sites and have been associated with patient survival. However, the mechanisms regulating MHC-II expression, particularly through genetic and epigenetic factors, are not yet fully understood. In this study, we identified a key signaling pathway involving the histone H2AK119 deubiquitinase BRCA1 associated protein 1 (BAP1), the interferon regulatory factor interferon regulatory factor 1 (IRF1), and the MHC-II transactivator class II transactivator (CIITA), which directly activates MHC-II gene expression.
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