: Hodgkin lymphoma (HL) accounts for 10% of lymphoma cases every year. HL is often curable by conventional chemotherapy and radiotherapy. However, in case of relapsed or refractory HL (r/r HL) after autologous hematopoietic stem cell transplantation (ASCT), few treatment options are currently available. Blockade of the immune checkpoint receptors, programmed death receptor-1 (PD-1), or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expressed on T-cells, and their ligands expressed on tumor-associated antigen-presenting cells (APCs), and Hodgkin and Reed/Sternberg (HRS) cells can remove inhibitory signals from anti-tumor T cells. Checkpoint blockade using monoclonal antibodies could be a potential treatment. Nivolumab and pembrolizumab are approved antibodies for the treatment of r/r HL.: This paper provides a comprehensive discussion of checkpoint inhibitors in HL treatment, including the most important clinical trials with mono- or combination therapies as a first or second-line treatment of HL.: Relatively high response rates and an acceptable safety profile of checkpoint inhibitors make them an effective therapy for HL. The combination of checkpoint inhibition with other conventional cancer treatments and identifying the mechanisms responsible for resistance to checkpoint inhibition may improve the efficacy and safety of this immunotherapy, and enhance patient quality of life.
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http://dx.doi.org/10.1080/14737140.2021.1918548 | DOI Listing |
J Transl Med
January 2025
Joint Research Center for Occupational Medicine and Health of IHM, School of Medicine, Anhui University of Science and Technology, Huainan, Anhui, 232000, China.
Background: PRDX2 is significantly expressed in various cancers and is associated with the proliferation of tumor cells. Nonetheless, the precise mechanism of PRDX2 in tumor immunity remains incompletely understood. This study aims to investigate the impact of PRDX2, which is highly expressed in lung adenocarcinoma, on T cells in the tumor immune microenvironment, and its immune action target to promote the immune escape of lung cancer cells, to provide a theoretical basis for lung adenocarcinoma treatment with PRDX2 as the target.
View Article and Find Full Text PDFNat Cancer
January 2025
Department of Cell Biology, Harvard Medical School, Boston, MA, USA.
Cancer cells frequently rewire their metabolism to support proliferation and evade immune surveillance, but little is known about metabolic targets that could increase immune surveillance. Here we show a specific means of mitochondrial respiratory complex I (CI) inhibition that improves tumor immunogenicity and sensitivity to immune checkpoint blockade (ICB). Targeted genetic deletion of either Ndufs4 or Ndufs6, but not other CI subunits, induces an immune-dependent growth attenuation in melanoma and breast cancer models.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Sonata Therapeutics Inc, Watertown, Massachusetts, USA
Cancer immunotherapy-including immune checkpoint inhibition (ICI) and adoptive cell therapy (ACT)-has become a standard, potentially curative treatment for a subset of advanced solid and liquid tumors. However, most patients with cancer do not benefit from the rapidly evolving improvements in the understanding of principal mechanisms determining cancer immune responsiveness (CIR); including patient-specific genetically determined and acquired factors, as well as intrinsic cancer cell biology. Though CIR is multifactorial, fundamental concepts are emerging that should be considered for the design of novel therapeutic strategies and related clinical studies.
View Article and Find Full Text PDFCancer Cell
January 2025
Cancer Systems Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK; Centre for Cancer Evolution, Bart's Cancer Institute, Queen Mary University London, London EC1M 6AU, UK. Electronic address:
Fewer than 50% of metastatic deficient mismatch repair (dMMR) colorectal cancer (CRC) patients respond to immune checkpoint inhibition (ICI). Identifying and expanding this patient population remains a pressing clinical need. Here, we report that an interferon-high immunophenotype locally enriched in cytotoxic lymphocytes and antigen-presenting macrophages is required for response.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
January 2025
Research Center for Preclinical Medicine, Southwest Medical University, Luzhou 646000, China.
Objectives: To explore the mechanism by which (PSD) inhibits invasion and metastasis of triple-negative breast cancer (TNBC).
Methods: The public databases were used to identify the potential targets of PSD and the invasion and metastasis targets of TNBC to obtain the intersection targets between PSD and TNBC. The "PSD-target-disease" interaction network was constructed and protein-protein interaction (PPI) analysis was performed to obtain the core targets, which were analyzed for KEGG pathway and GO functional enrichment.
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