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      Associations of Tumor PD-1 Ligands, Immunohistochemical Studies, and Textural Features in 18F-FDG PET in Squamous Cell Carcinoma of the Head and Neck

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          Abstract

          To know tumor PD-L1 expression through IHC or the FDG-PET related radiomics, we investigated the association between programmed cell death protein 1 ligand (PD-L1) expression and immunohistochemical (IHC) biomarkers or textural features of 18F-fluoro-2-deoxdeoxyglucose positron emission tomography ( 18F-FDG PET) in 53 oropharyngeal or hypopharyngeal cancer patients who were ready to undergo radiotherapy-based treatment. Differences in textural features or biomarkers between tumors with and without PD-L1 expression were tested using a Mann–Whitney U test. The predicted values for PD-L1 expression were examined using logistic regression analysis. The mean percentages of tumor PD-L1 expression were 6.2 ± 13.5. Eighteen tumors had PD-L1 expression ≥5%, whereas 30 tumors ≥1%. Using a 5% cutoff, the p16 staining percentage and the textural index of correlation were two factors associated with PD-L1 expression. The odds ratios (ORs) were 17.00 ( p = 0.028) and 0.009 ( p = 0.015), respectively. When dichotomizing PD-L1 at 1%, the p16 and Ki-67 staining percentages were two predictors for PD-L1 expression with ORs of 11.41 ( p = 0.035) and 757.77 ( p = 0.045). p16 and Ki-67 staining percentages and several PET/CT-derived textural features can provide supplemental information to determine tumor PD-L1 expression in HNCs.

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          The blockade of immune checkpoints in cancer immunotherapy.

          Drew M Pardoll (2012)
          Among the most promising approaches to activating therapeutic antitumour immunity is the blockade of immune checkpoints. Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. It is now clear that tumours co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumour antigens. Because many of the immune checkpoints are initiated by ligand-receptor interactions, they can be readily blocked by antibodies or modulated by recombinant forms of ligands or receptors. Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibodies were the first of this class of immunotherapeutics to achieve US Food and Drug Administration (FDA) approval. Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses.
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            Activation of the PD-1 pathway contributes to immune escape in EGFR-driven lung tumors.

            Esra A Akbay, Shohei Koyama, Julian Carretero … (2013)
            The success in lung cancer therapy with programmed death (PD)-1 blockade suggests that immune escape mechanisms contribute to lung tumor pathogenesis. We identified a correlation between EGF receptor (EGFR) pathway activation and a signature of immunosuppression manifested by upregulation of PD-1, PD-L1, CTL antigen-4 (CTLA-4), and multiple tumor-promoting inflammatory cytokines. We observed decreased CTLs and increased markers of T-cell exhaustion in mouse models of EGFR-driven lung cancer. PD-1 antibody blockade improved the survival of mice with EGFR-driven adenocarcinomas by enhancing effector T-cell function and lowering the levels of tumor-promoting cytokines. Expression of mutant EGFR in bronchial epithelial cells induced PD-L1, and PD-L1 expression was reduced by EGFR inhibitors in non-small cell lung cancer cell lines with activated EGFR. These data suggest that oncogenic EGFR signaling remodels the tumor microenvironment to trigger immune escape and mechanistically link treatment response to PD-1 inhibition. We show that autochthonous EGFR-driven lung tumors inhibit antitumor immunity by activating the PD-1/PD-L1 pathway to suppress T-cell function and increase levels of proinflammatory cytokines. These findings indicate that EGFR functions as an oncogene through non-cell-autonomous mechanisms and raise the possibility that other oncogenes may drive immune escape. ©2013 AACR.
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              A mechanism of hypoxia-mediated escape from adaptive immunity in cancer cells.

              Ivraym Barsoum, Chelsea Smallwood, D Siemens … (2014)
              Immune escape is a fundamental trait of cancer in which mechanistic knowledge is incomplete. Here, we describe a novel mechanism by which hypoxia contributes to tumoral immune escape from cytotoxic T lymphocytes (CTL). Exposure of human or murine cancer cells to hypoxia for 24 hours led to upregulation of the immune inhibitory molecule programmed cell death ligand-1 (PD-L1; also known as B7-H1), in a manner dependent on the transcription factor hypoxia-inducible factor-1α (HIF-1α). In vivo studies also demonstrated cellular colocalization of HIF-1α and PD-L1 in tumors. Hypoxia-induced expression of PD-L1 in cancer cells increased their resistance to CTL-mediated lysis. Using glyceryl trinitrate (GTN), an agonist of nitric oxide (NO) signaling known to block HIF-1α accumulation in hypoxic cells, we prevented hypoxia-induced PD-L1 expression and diminished resistance to CTL-mediated lysis. Moreover, transdermal administration of GTN attenuated tumor growth in mice. We found that higher expression of PD-L1 induced in tumor cells by exposure to hypoxia led to increased apoptosis of cocultured CTLs and Jurkat leukemia T cells. This increase in apoptosis was prevented by blocking the interaction of PD-L1 with PD-1, the PD-L1 receptor on T cells, or by addition of GTN. Our findings point to a role for hypoxia/HIF-1 in driving immune escape from CTL, and they suggest a novel cancer immunotherapy to block PD-L1 expression in hypoxic-tumor cells by administering NO mimetics.
              Article 0 comments Cited 306 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Shang-Wen Chen: vincent1680616@yahoo.com.tw
                Chia-Hung Kao: d10040@mail.cmuh.org.tw
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 8 January 2018
                Publication date PMC-release: 8 January 2018
                Publication date Collection: 2018
                Volume: 8
                Electronic Location Identifier: 105
                Affiliations
                [1 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Department of Pathology, , China Medical University Hospital, ; Taichung, Taiwan
                [2 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Department of Radiation Oncology, , China Medical University Hospital, ; Taichung, Taiwan
                [3 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, The Ph.D. Program for Cancer Biology and Drug Discovery, , China Medical University and Academia Sinica, ; Taichung, Taiwan
                [4 ]ISNI 0000 0000 9263 9645, GRID grid.252470.6, Department of Computer Science and Information Engineering, , Asia University, ; Taichung, Taiwan
                [5 ]ISNI 0000 0004 0572 9415, GRID grid.411508.9, Department of Nuclear Medicine and PET Center, , China Medical University Hospital, ; Taichung, Taiwan
                [6 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, Department of Biomedical Imaging and Radiological Science, , China Medical University, ; Taichung, Taiwan
                [7 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, School of Medicine, , China Medical University, ; Taichung, Taiwan
                [8 ]ISNI 0000 0000 9337 0481, GRID grid.412896.0, School of Medicine, , Taipei Medical University, ; Taipei, Taiwan
                [9 ]ISNI 0000 0001 0083 6092, GRID grid.254145.3, Graduate Institute of Clinical Medical Science, , School of Medicine, College of Medicine, China Medical University, ; Taichung, Taiwan
                [10 ]ISNI 0000 0000 9263 9645, GRID grid.252470.6, Department of Bioinformatics and Medical Engineering, , Asia University, ; Taichung, Taiwan
                Article
                Publisher ID: 18489
                DOI: 10.1038/s41598-017-18489-2
                PMC ID: 5758832
                PubMed ID: 29311707
                SO-VID: 46640b84-a6d3-48cf-b6a3-1274f2d046c0
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 9 October 2017
                Date accepted : 12 December 2017
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2018

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