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Journal articles on the topic 'Immunology; Tumour cells'

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1

Alotaibi, Faizah, Mark Vincent, Weiping Min, and James Koropatnick. "498 Downregulation of CD5 in CD8+ T tumour-infiltrating lymphocytes associates with increased level of activation and exhaustion." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A533. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0498.

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BackgroundCD5, a member of the scavenger receptor cysteine-rich superfamily, is a marker for T cells and a subset of B cells (B1a). CD5 associates with T-cell and B-cell receptors and impair TCR signaling1 2 and increased CD5 is an indication of B cell activation. Furthermore, CD5 levels on CD8+ T cell splenocytes were significantly increased after TCR/CD3 stimulation using ex vivo treatment with anti-CD3/anti-CD28 MAbs compared to non-stimulated CD8+ T splenocytes.3 Previous studies have shown a correlation between CD5 and anti-tumour immunity where CD5 knockout mice inoculated with B16F10 me
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2

Ahmad, Sharon. "Tumour cells tout trogocytosis." Nature Reviews Immunology 7, no. 4 (2007): 250–51. http://dx.doi.org/10.1038/nri2068.

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3

Cerundolo, Vincenzo. "Tumour immunology: T cells work together to fight cancer." Current Biology 9, no. 18 (1999): R695—R697. http://dx.doi.org/10.1016/s0960-9822(99)80442-4.

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4

Eyileten, Ceren, Kinga Majchrzak, Zofia Pilch, et al. "Immune Cells in Cancer Therapy and Drug Delivery." Mediators of Inflammation 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/5230219.

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Recent studies indicate the critical role of tumour associated macrophages, tumour associated neutrophils, dendritic cells, T lymphocytes, and natural killer cells in tumourigenesis. These cells can have a significant impact on the tumour microenvironment via their production of cytokines and chemokines. Additionally, products secreted from all these cells have defined specific roles in regulating tumour cell proliferation, angiogenesis, and metastasis. They act in a protumour capacityin vivoas evidenced by the recent studies indicating that macrophages, T cells, and neutrophils may be manipul
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5

Real, Carla, Francisco Caiado, Catia Igreja, et al. "Delta Like 4 Expressing Bone Marrow-Derived Endothelial Progenitor Cells Regulate Tumour Angiogenesis." Blood 110, no. 11 (2007): 3728. http://dx.doi.org/10.1182/blood.v110.11.3728.3728.

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Abstract Bone marrow-derived endothelial progenitor cells (BM-EPCs) have been implicated in adult neoangiogenesis and consequently used as therapies for human pathologies with endothelial damage. The administration of these cells in human patients temporally improves endothelial function, although the engraftment of these cells in newly formed vessels is inefficient. Conversely, therapeutic stratagies to block EPC contribution during tumor angiogenesis have been proposed. In this work, we analysed the role of the Notch/Delta signalling pathway in EPC function during tumour neoangiogenesis, by
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6

Schröder, Sabine, Simone Broese, Jana Baake, et al. "Effect of Ionizing Radiation on Human EA.hy926 Endothelial Cells under Inflammatory Conditions and Their Interactions with A549 Tumour Cells." Journal of Immunology Research 2019 (September 2, 2019): 1–14. http://dx.doi.org/10.1155/2019/9645481.

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Purpose. Most tumours are characterized by an inflammatory microenvironment, and correlations between inflammation and cancer progression have been shown. Endothelial cells (ECs), as part of the tumour microenvironment, play a crucial role in inflammatory processes as well as in angiogenesis and could be critical targets of cancer therapy like irradiation. Therefore, in the present study we investigated the effect of ionizing radiation on endothelial cells under inflammatory conditions and their interactions with tumour cells. Methods. Nonactivated and TNF-α treatment-activated human EC EA.hy9
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7

Bordon, Yvonne. "Macrophages throw tumour cells a lifeline." Nature Reviews Immunology 19, no. 4 (2019): 202–3. http://dx.doi.org/10.1038/s41577-019-0148-1.

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8

Ashman, Leonie K. "The immunogenicity of tumour cells." Immunology and Cell Biology 65, no. 4 (1987): 271–77. http://dx.doi.org/10.1038/icb.1987.31.

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9

Carpenter, Ben, Sara Ghorashian, Emma Nicholson, et al. "Targeting Therapeutic T Cells to Tumour Niches." Blood 120, no. 21 (2012): 3009. http://dx.doi.org/10.1182/blood.v120.21.3009.3009.

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Abstract Abstract 3009 Background: Interactions between tumour cells and host cells within the microenvironment are important in promoting the development of cancer. Tumor niches provide crucial anti-apoptotic and anti-proliferative signals that drive tumor chemoresistance. The CXCR4-CXCL12 chemokine axis forms a critical component of this niche. CXCL12 produced by stromal cells has direct pro-survival effects upon tumor cells, promotes metastasis and recruits CXCR4-expressing regulatory T cell populations that block anti-tumour immunity. In this study, we have tested the hypothesis that targe
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10

Battke, Christina, Romana Ruiss, Ulrich Welsch, et al. "Tumour exosomes inhibit binding of tumour-reactive antibodies to tumour cells and reduce ADCC." Cancer Immunology, Immunotherapy 60, no. 5 (2011): 639–48. http://dx.doi.org/10.1007/s00262-011-0979-5.

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11

Gasser, Stephan, Lina H. K. Lim, and Florence S. G. Cheung. "The role of the tumour microenvironment in immunotherapy." Endocrine-Related Cancer 24, no. 12 (2017): T283—T295. http://dx.doi.org/10.1530/erc-17-0146.

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Recent success in immunomodulating strategies in lung cancer and melanoma has prompted much enthusiasm in their potential to treat other advanced solid malignancies. However, their applications have shown variable success and are even ineffective against some tumours. The efficiency of immunotherapies relies on an immunogenic tumour microenvironment. The current field of cancer immunology has focused on understanding the interaction of cancer and host immune cells to break the state of immune tolerance and explain how molecular patterns of cytokines and chemokines affect tumour progression. He
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12

Ishida, A., H. Tanaka, T. Hiura, et al. "Generation of Anti-tumour Effector T Cells from Naïve T Cells by Stimulation with Dendritic/tumour Fusion Cells." Scandinavian Journal of Immunology 66, no. 5 (2007): 546–54. http://dx.doi.org/10.1111/j.1365-3083.2007.02012.x.

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13

Zou, Weiping, and Nicholas P. Restifo. "TH17 cells in tumour immunity and immunotherapy." Nature Reviews Immunology 10, no. 4 (2010): 248–56. http://dx.doi.org/10.1038/nri2742.

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14

Knight, Stella C. "Dendritic cells as initiators of tumour immunity." Immunology Today 16, no. 11 (1995): 547. http://dx.doi.org/10.1016/0167-5699(95)80050-6.

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15

LAW, S. K. A. "Antigen shedding and metastasis of tumour cells." Clinical & Experimental Immunology 85, no. 1 (2008): 1–2. http://dx.doi.org/10.1111/j.1365-2249.1991.tb05672.x.

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16

Ward, Stephen, David Casey, Marie-Christine Labarthe, et al. "Immunotherapeutic potential of whole tumour cells." Cancer Immunology, Immunotherapy 51, no. 7 (2002): 351–57. http://dx.doi.org/10.1007/s00262-002-0286-2.

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17

Ogino, Shuji, Jonathan A. Nowak, Tsuyoshi Hamada, et al. "Integrative analysis of exogenous, endogenous, tumour and immune factors for precision medicine." Gut 67, no. 6 (2018): 1168–80. http://dx.doi.org/10.1136/gutjnl-2017-315537.

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Immunotherapy strategies targeting immune checkpoints such as the CTLA4 and CD274 (programmed cell death 1 ligand 1, PD-L1)/PDCD1 (programmed cell death 1, PD-1) T-cell coreceptor pathways are revolutionising oncology. The approval of pembrolizumab use for solid tumours with high-level microsatellite instability or mismatch repair deficiency by the US Food and Drug Administration highlights promise of precision immuno-oncology. However, despite evidence indicating influences of exogenous and endogenous factors such as diet, nutrients, alcohol, smoking, obesity, lifestyle, environmental exposur
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18

Hokland, Marianne, Mikkel S. Petersen, Charlotte C. Fleischer, et al. "Tumor Localization and Quantitation of Adoptively Transfered T Lymphocytes in a Murine Model." Blood 104, no. 11 (2004): 1343. http://dx.doi.org/10.1182/blood.v104.11.1343.1343.

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Abstract Tracking adoptively transferred antigen-specific T lymphocytes is an important prerequisite for devising better protocols for cellular therapy. To this end we have developed a highly sensitive method for “in situ” visualization of labelled lymphocytes in vivo by combined PET and magnetic resonance imaging (MRI) to monitor the distribution of adoptively transferred tumour-specific T cells in a mouse model system. Moreover, quantitation of the adoptively transferred cells in tumor was performed by flow cytometry. C57BL/6J mice carrying subcutaneous tumours of the ovalbumin (OVA)-express
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19

Sharonov, George V., Ekaterina O. Serebrovskaya, Diana V. Yuzhakova, Olga V. Britanova, and Dmitriy M. Chudakov. "B cells, plasma cells and antibody repertoires in the tumour microenvironment." Nature Reviews Immunology 20, no. 5 (2020): 294–307. http://dx.doi.org/10.1038/s41577-019-0257-x.

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20

Le Pape, A., C. Jubault, R. Barot-Clorbaru, M. Musset, and G. Mathé. "Targetting of immunocompetent cells for tumour scintigraphy." International Journal of Immunopharmacology 10 (January 1988): 29. http://dx.doi.org/10.1016/0192-0561(88)90229-9.

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21

Soars, Diane, Angus G. Dalgleish, Alan A. Melcher, et al. "Heated tumour cells of autologous and allogeneic origin elicit anti-tumour immunity." Cancer Immunology, Immunotherapy 53, no. 4 (2004): 323–30. http://dx.doi.org/10.1007/s00262-003-0452-1.

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22

Mahnke, Yolanda D., Jochen Schwendemann, Philipp Beckhove, and Volker Schirrmacher. "Maintenance of long-term tumour-specific T-cell memory by residual dormant tumour cells." Immunology 115, no. 3 (2005): 325–36. http://dx.doi.org/10.1111/j.1365-2567.2005.02163.x.

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23

Minton, Kirsty. "B cells lead the way in tumour progression." Nature Reviews Immunology 5, no. 7 (2005): 517. http://dx.doi.org/10.1038/nri1653.

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24

Zou, Weiping, and Nicholas P. Restifo. "Erratum: TH17 cells in tumour immunity and immunotherapy." Nature Reviews Immunology 11, no. 8 (2011): 565. http://dx.doi.org/10.1038/nri3029.

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25

Jackson, Andrew M., M. A. Chambers, P. J. Selby, and G. Packham. "Apoptosis of tumour cells during infection with mycobacteria." Immunology Letters 56 (May 1997): 444. http://dx.doi.org/10.1016/s0165-2478(97)86805-8.

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26

Raffaghello, Lizzia, and Francesco Dazzi. "Classification and biology of tumour associated stromal cells." Immunology Letters 168, no. 2 (2015): 175–82. http://dx.doi.org/10.1016/j.imlet.2015.06.016.

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27

Gottfried, E., M. Kreutz, S. Haffner, et al. "Differentiation of Human Tumour-associated Dendritic Cells into Endothelial-like Cells: An Alternative Pathway of Tumour Angiogenesis." Scandinavian Journal of Immunology 65, no. 4 (2007): 329–35. http://dx.doi.org/10.1111/j.1365-3083.2007.01903.x.

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28

Vauleon, Elodie, Tony Avril, Brigitte Collet, Jean Mosser, and Véronique Quillien. "Overview of Cellular Immunotherapy for Patients with Glioblastoma." Clinical and Developmental Immunology 2010 (2010): 1–18. http://dx.doi.org/10.1155/2010/689171.

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High grade gliomas (HGG) including glioblastomas (GBM) are the most common and devastating primary brain tumours. Despite important progresses in GBM treatment that currently includes surgery combined to radio- and chemotherapy, GBM patients' prognosis remains very poor. Immunotherapy is one of the new promising therapeutic approaches that can specifically target tumour cells. Such an approach could also maintain long term antitumour responses without inducing neurologic defects. Since the past 25 years, adoptive and active immunotherapies using lymphokine-activated killer cells, cytotoxic T c
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29

Byrne, Scott N., and Gary M. Halliday. "Dendritic cells: Making progress with tumour regression?" Immunology and Cell Biology 80, no. 6 (2002): 520–30. http://dx.doi.org/10.1046/j.1440-1711.2002.01122.x.

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30

Albertsson, Per A., Per H. Basse, Marianne Hokland, et al. "NK cells and the tumour microenvironment: implications for NK-cell function and anti-tumour activity." Trends in Immunology 24, no. 11 (2003): 603–9. http://dx.doi.org/10.1016/j.it.2003.09.007.

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31

Semiglazov, V. F., A. I. Tseluiko, I. A. Baldueva, et al. "Immunology and immunotherapy in the complex treatment of malignant tumors." Meditsinskiy sovet = Medical Council, no. 4 (April 20, 2021): 248–57. http://dx.doi.org/10.21518/2079-701x-2021-4-248-257.

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Immuno-oncology is a rapidly developing field in medicine. Drug combination therapies have already been studied in many clinical trials of different types of tumours. In recent years, a checkpoint inhibition therapy with monoclonal antibodies that target cytological T-lymphocytes has been developed. Thus, inhibition of two regulator genes CTLA 4 and PD1 or PD-L1 ligand to it is able to restore mediated T-cell tumour regression in its many localizations. The article considers a number of key fields of immunology and immunotherapy through a specific example of breast cancer (BC): the role of T-l
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32

Redzovic, Arnela, Gordana Laskarin, Marin Dominovic, Herman Haller, and Daniel Rukavina. "Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface." Clinical and Developmental Immunology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/542152.

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During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) enhances the already established tolerogenic features of decidual dendritic cells with the inability to progress towards Th1 immune orientation due to lowered interferon (IFN)-γand interleukin (IL)-15 expression. Mucine 1 (Muc 1) supports alternative activation of decidual macrophages, restricts the
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33

Sapega, O., R. Mikyskova, K. Musilek, J. Bieblova, Z. Hodny, and M. Reinis. "P01.16 Effects of the STAT3 inhibitors on senescent tumour cells." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (2020): A16.1—A16. http://dx.doi.org/10.1136/jitc-2020-itoc7.29.

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BackgroundCellular senescence is the process of cell proliferation arrest. Premature cellular senescence can be induced by chemotherapy, irradiation and, under certain circumstances, by cytokines. Senescent cells produce a number of secreted proteins and growth factors that may either stimulate or inhibit cell proliferation. One of the major cytokines that play role in regulation of cellular senescence is IL-6. IL-6/STAT3 signaling pathway represent decisive regulatory factors in cellular senescence. The objective of this study was to compare the effects of the STAT3 inhibitors on senescent an
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34

Turley, Shannon J., Viviana Cremasco, and Jillian L. Astarita. "Immunological hallmarks of stromal cells in the tumour microenvironment." Nature Reviews Immunology 15, no. 11 (2015): 669–82. http://dx.doi.org/10.1038/nri3902.

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35

Schmidt-Arras, Dirk, Eithan Galun, and Stefan Rose-John. "The two facets of gp130 signalling in liver tumorigenesis." Seminars in Immunopathology 43, no. 4 (2021): 609–24. http://dx.doi.org/10.1007/s00281-021-00861-0.

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AbstractThe liver is a vital organ with multiple functions and a large regenerative capacity. Tumours of the liver are the second most frequently cause of cancer-related death and develop in chronically inflamed livers. IL-6-type cytokines are mediators of inflammation and almost all members signal via the receptor subunit gp130 and the downstream signalling molecule STAT3. We here summarize current knowledge on how gp130 signalling and STAT3 in tumour cells and cells of the tumour micro-environment drives hepatic tumorigenesis. We furthermore discuss very recent findings describing also anti-
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36

Matos Pires, Eugénia, and Cecília Moura. "Immune Response in Melanoma: A Basis to Understand the Role of Immunotherapy with Immune Checkpoint Inhibitors." Journal of the Portuguese Society of Dermatology and Venereology 76, no. 1 (2018): 47–52. http://dx.doi.org/10.29021/spdv.76.1.868.

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The knowledge of the pathophysiology of tumour progression is crucial to understand the therapeutic targets in order to control the disease. The mechanisms used by the immune system to affect cancer development and progression has been a challenging question in immunology. It is now postulated that immunology plays a dual role in this process: it protects against tumour growth, destroying “aberrant” tumour cells, but may also promote tumour progression by selecting tumour cells that are able to escape the immune response and survive in an immunocompetent host. These findings gave rise to the c
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37

Hacker, Ulrich T., Ines Schildhauer, Margarita C. Barroso, et al. "Gene transfer preferentially selects MHC class I positive tumour cells and enhances tumour immunogenicity." Cancer Immunology, Immunotherapy 55, no. 5 (2005): 547–57. http://dx.doi.org/10.1007/s00262-005-0035-4.

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38

Hughes, Ellyn, Sarah N. Lauder, Kathryn Smart, et al. "Primary breast tumours but not lung metastases induce protective anti-tumour immune responses after Treg-depletion." Cancer Immunology, Immunotherapy 69, no. 10 (2020): 2063–73. http://dx.doi.org/10.1007/s00262-020-02603-x.

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Abstract Although metastatic disease is responsible for the majority of cancer deaths, tests of novel immunotherapies in mouse tumour models often focus on primary tumours without determining whether these therapies also target metastatic disease. This study examined the impact of depleting Foxp3+ regulatory T cells (Treg), on lung metastases, using a mouse model of breast cancer. After Treg-depletion, generation of an immune response to the primary tumour was a critical determinant for limiting development of metastasis. Indeed, resection of the primary tumour abrogated any effect of Treg-dep
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39

Mulder, Wilhelmina M. C., Marij J. Stukart, Micha Roos, et al. "Culture of tumour-infiltrating lymphocytes from melanoma and colon carcinoma: removal of tumour cells does not affect tumour-specificity." Cancer Immunology, Immunotherapy 41, no. 5 (1995): 293–301. http://dx.doi.org/10.1007/s002620050231.

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40

Mulder, Wilhelmina M. C., Marij J. Stukart, Micha Roos, et al. "Culture of tumour-infiltrating lymphocytes from melanoma and colon carcinoma: Removal of tumour cells does not affect tumour-specificity." Cancer Immunology, Immunotherapy 41, no. 5 (1995): 293–301. http://dx.doi.org/10.1007/bf01517217.

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41

Du Toit, Andrea. "Tumour cells show off bacterial peptides." Nature Reviews Microbiology 19, no. 5 (2021): 284. http://dx.doi.org/10.1038/s41579-021-00551-6.

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42

Shklovskaya, Elena, Alexandra M. Terry, Thomas V. Guy, et al. "Tumour‐specific CD4 T cells eradicate melanoma via indirect recognition of tumour‐derived antigen." Immunology & Cell Biology 94, no. 6 (2016): 593–603. http://dx.doi.org/10.1038/icb.2016.14.

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43

Fares, Jawad, Ilya Ulasov, Peter Timashev, and Maciej S. Lesniak. "Emerging principles of brain immunology and immune checkpoint blockade in brain metastases." Brain 144, no. 4 (2021): 1046–66. http://dx.doi.org/10.1093/brain/awab012.

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Abstract Brain metastases are the most common type of brain tumours, harbouring an immune microenvironment that can in principle be targeted via immunotherapy. Elucidating some of the immunological intricacies of brain metastases has opened a therapeutic window to explore the potential of immune checkpoint inhibitors in this globally lethal disease. Multiple lines of evidence suggest that tumour cells hijack the immune regulatory mechanisms in the brain for the benefit of their own survival and progression. Nonetheless, the role of the immune checkpoint in the complex interplays between cancer
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44

HARRIS, C. L., K. S. KAN, G. T. STEVENSON, and B. P. MORGAN. "Tumour cell killing using chemically engineered antibody constructs specific for tumour cells and the complement inhibitor CD59." Clinical & Experimental Immunology 107, no. 2 (1997): 364–71. http://dx.doi.org/10.1111/j.1365-2249.1997.265-ce1156.x.

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45

Gaken, Joop, Louisa Pericleous, Farzin Farzaneh, Ghulam J. Mufti, and Mahvash Tavassoli. "TAT-Apoptin Mediated Induction of Apoptosis in Leukaemic Cells." Blood 108, no. 11 (2006): 1900. http://dx.doi.org/10.1182/blood.v108.11.1900.1900.

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Abstract We have studied the specific targeting of leukaemic cells using the Chicken Anaemia Virus (CAV)-derived protein VP3 (Apoptin) linked to the protein transduction domain (PTD) from HIV TAT with the aim of using this strategy for in vitro purging. Apoptin is a 13.6 kDa protein which induces apoptosis specifically in cancer cells whilst leaving normal cells unaffected. Expression of Apoptin in normal cells results in its cytoplasmic localisation. In tumour cells Apoptin resides initially in the cytoplasm and subsequently translocates to the nucleus and induces apoptosis. Apoptin is phosph
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46

Webb, Steven D., Jonathan A. Sherratt, and Reginald G. Fish. "Cells behaving badly: a theoretical model for the Fas/FasL system in tumour immunology." Mathematical Biosciences 179, no. 2 (2002): 113–29. http://dx.doi.org/10.1016/s0025-5564(02)00120-7.

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47

De Weger, R. A., H. F. J. Dullens, R. J. De Boer, and W. Den Otter. "Mathematical analysis of the cellular immune reaction against tumour cells." Immunology Today 6, no. 11 (1985): 316–17. http://dx.doi.org/10.1016/0167-5699(85)90119-7.

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48

Davern, Maria, Joanne Lysaght, Andrew Sheppard, et al. "776 A role for immune checkpoint blockade to enhance T cell-mediated responses in combination with chemotherapy in oesophageal adenocarcinoma." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A826—A827. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0776.

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BackgroundCombining immune checkpoint inhibitors (ICIs) with immunogenic chemotherapies is a promising approach in oesophageal adenocarcinoma (OAC) to convert ‘cold’ tumours to ‘hot’ tumours expanding the efficacy of ICIs to a greater spectrum of patients.1 However, there is a vast array of immune checkpoints (ICs) expressed by T cells and the effect of ICIs in combination with chemotherapy regimens is largely unknown.2MethodsThe expression profile of a range of ICs on circulating and tumour-infiltrating T cells was assessed using flow cytometry prior to and post-neoadjuvant treatment and corr
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49

Martinez-Usatorre, A., E. Kadioglu, C. Cianciaruso, et al. "O4 Mechanisms of lung cancer hyper-progression promoted by PD-1 immune checkpoint blockade." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (2020): A5.1—A5. http://dx.doi.org/10.1136/jitc-2020-itoc7.9.

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BackgroundImmune checkpoint blockade (ICB) with antibodies against PD-1 or PD-L1 may provide therapeutic benefits in patients with non-small cell lung cancer (NSCLC). However, most tumours are resistant and cases of disease hyper-progression have also been reported.Materials and MethodsGenetically engineered mouse models of KrasG12Dp53null NSCLC were treated with cisplatin along with antibodies against angiopoietin-2/VEGFA, PD-1 and CSF1R. Tumour growth was monitored by micro-computed tomography and the tumour vasculature and immune cell infiltrates were assessed by immunofluorescence staining
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50

Cendrowicz, E., LJ Jacob, S. Greenwald, et al. "P01.09 Dual signalling protein 107 triggers innate and adaptive immune response towards tumour cells." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (2020): A12—A13. http://dx.doi.org/10.1136/jitc-2020-itoc7.22.

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BackgroundDual signalling protein 107 (DSP107) is a trimeric fusion protein consisting of the extracellular domains of human SIRPα and 4-1BBL. SIRPα binds to CD47, frequently overexpressed on cancer cells, and 41BBL binds to 41BB on activated T-cells. The SIRPα domain triggers the innate immune response by inhibiting the CD47/SIRPα ‘don’t eat me’ signalling. It thus promotes phagocytosis of cancer cells by granulocytes, macrophages and dendritic cells. With its other side, 41BBL domain binds to pre-activated T cells and stimulates their expansion, cytokine production and cytolytic effector fun
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