Relevant bibliographies by topics / Immunology; Tumour cells

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Immunology; Tumour cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Immunology; Tumour cells"

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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 (November 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 melanoma cells had delayed tumour growth compared to wild type mice.4 In tumour-infiltrating lymphocytes (TILs) isolated from lung cancer patients, CD5 levels were negatively correlated with anti-tumour activity and tumour-mediated activation-induced T cell death,5 suggesting that CD5 could impair activation of anti-tumour T cells. However, the correlation between CD5 level expression and T cell activation and exhaustion in the tumour microenvironment and in peripheral organs is ill-defined and requires further investigation.MethodsWe determined CD5 levels in T cell subsets in different organs in mice bearing syngeneic 4T1 breast tumour homografts and assessed the relationship between CD5 and increased CD69 and PD-1 (markers of T cell activation and exhaustion) by flow cytometry.ResultsWe report that T cell CD5 levels were higher in CD4+ T cells than in CD8+ T cells in 4T1 tumour-bearing mice, and that high CD5 levels on CD4+ T cells were maintained in peripheral organs (spleen and lymph nodes). However, both CD4+ and CD8+ T cells recruited to tumours had reduced CD5 compared to CD4+ and CD8+ T cells in peripheral organs. In addition, CD5highCD4+ T cells and CD5highCD8+ T cells from peripheral organs exhibited higher levels of activation and associated exhaustion compared to CD5lowCD4+ T cell and CD5lowCD8+ T cell from the same organs. Interestingly, CD8+ T cells among TILs and downregulated CD5 were activated to a higher level, with concomitantly increased exhaustion markers, than CD8+CD5+ TILs.ConclusionsThus, differential CD5 levels among T cells in tumours and lymphoid organs can be associated with different levels of T cell activation and exhaustion, suggesting that CD5 may be a therapeutic target for immunotherapeutic activation in cancer therapy.AcknowledgementsThe author thanks Rene Figueredo and Ronak Zareardalan for their assistance in animal workEthics ApprovalThis study was approved by the Animal Use Subcommittee of the University of Western OntarioReferencesAzzam HS, et al., Fine tuning of TCR signaling by CD5. The Journal of Immunology 2001. 166(9): p. 5464–5472.Voisinne GA, Gonzalez de Peredo and Roncagalli R. CD5, an undercover regulator of TCR signaling. Frontiers in Immunology 2018;9:p. 2900.Alotaibi, F., et al., CD5 blockade enhances ex vivo CD8+ T cell activation and tumour cell cytotoxicity. European journal of immunology 2020;50(5): p. 695–704.Tabbekh, M., et al., Rescue of tumor-infiltrating lymphocytes from activation-induced cell death enhances the antitumor CTL response in CD5-deficient mice. The Journal of Immunology, 2011. 187(1): p. 102–109.Dorothée, G., et al., In situ sensory adaptation of tumor-infiltrating T lymphocytes to peptide-MHC levels elicits strong antitumor reactivity. The Journal of Immunology 2005;174(11): p. 6888–6897.
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Ahmad, Sharon. "Tumour cells tout trogocytosis." Nature Reviews Immunology 7, no. 4 (April 2007): 250–51. http://dx.doi.org/10.1038/nri2068.

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

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Eyileten, Ceren, Kinga Majchrzak, Zofia Pilch, Katarzyna Tonecka, Joanna Mucha, Bartlomiej Taciak, Katarzyna Ulewicz, 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 manipulated to exhibit cytotoxic activity against tumours. Therefore therapy targeting these cells may be promising, or they may constitute drug or anticancer particles delivery systems to the tumours. Herein, we discussed all these possibilities that may be used in cancer treatment.
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Real, Carla, Francisco Caiado, Catia Igreja, Ana P. Elias, Cristina Borges, Antonio Duarte, and Sergio Dias. "Delta Like 4 Expressing Bone Marrow-Derived Endothelial Progenitor Cells Regulate Tumour Angiogenesis." Blood 110, no. 11 (November 16, 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 regulating the expression of Notch ligand, delta-like 4 (Dll4) in these cells. Sublethally irradiated NOD-SCID mice received WT, Dll4+/− (Dll4 heterozygous mice) or Dll4 SiRNA-treated BM-EPCs and were subcutaneously inoculated with well established Human or murine tumor xenografts. Tumours growing in Dll4-depleted EPCs transplanted mice presented increased microvessel density when compared with WT EPCs transplanted mice or non-transplanted controls, regardless of VEGF expression. Although with increased vessel number, tumours of Dll4+/− EPC transplanted mice presented increased hypoxia and decreased tumour cell proliferation, suggesting an impairment in vessel function. In addition, these tumours present a diminished expression of PDGF, a vessel stabilizing factor, and increased expression of Ang2, known as a vessel destabilizing factor. We next verified whether the vessel destabilization observed in tumors after Dll4-depleted EPCs transplant might be due to a diferential endothelial differentiation or incorporation of EPCs in the tumour vasculature. In order to answer this question we quantified the incorporation of WT and Dll4-depleted EPCs in tumour vessels. Accordingly to our results, the presence of Dll4-depleted EPCs was reduced compared to WT EPCs, suggesting that Dll4-depleted EPCs might have reduced capacity to adhere to the renewing tumor vasculature, or to the underlying basement membrane. To test this, we used an in vitro endothelial differentiation assay, and observed a defect on the adhesion of of Dll4-depleted EPCs to extracellular matrix, which was correlated with a reduced expression of integrin subunits a3 and b1. These results suggest that the reduction of Dll4 on EPCs reduces integrin expression interfering with their ability to adhere, incorporate and stabilize the tumor vasculature during tumor neoangiogenesis. Therefore, EPCs have a major role in vessel stabilization in active neoangiogenic sites by the regulation of Dll4 expression. We propose that targeting the Notch/Dll4 pathway on EPCs, modulating vessel stability, may have therapeutic potential.
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Schröder, Sabine, Simone Broese, Jana Baake, Dajana Juerß, Stephan Kriesen, Guido Hildebrandt, and Katrin Manda. "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.hy926 were irradiated with doses between 0.1 Gy and 6 Gy with a linear accelerator. Using a multiplex assay, the accumulation of various chemokines (IL-8, MCP-1, E-selectin, and P-selectin) and soluble adhesion molecules (sICAM-1 and VCAM-1) as well as protein values of the vascular endothelial growth factor (VEGF) was measured in the supernatant at different time points. The adhesion capability of irradiated and nonirradiated A549 tumour cells to EA.hy926 cells was measured using flow cytometry, and the migration of tumour cells was investigated with a scratch motility assay. Results. In contrast to unirradiated cells, IR of ECs resulted in a modified release of chemokines IL-8 and MCP-1 as well as the adhesion molecules sICAM-1 and VCAM-1 in the EC, whereas concentrations of E-selectin and P-selectin as well as VEGF were not influenced. IR always affected the adhesion capability of tumour cells to ECs with the effect dependent on the IR-treated cell type. TNF-α treatment generally increased adhesion ability of the tumour cells. Tumour cell migration was clearly inhibited after IR. This inhibitory effect was eliminated for radiation doses from 0.5 to 2 Gy when, additionally, an inflammatory environment was predominant. Conclusions. Our results support past findings suggesting that ECs, as part of the inflammatory microenvironment of tumours, are important regulators of the actual tumour response to radiation therapy.
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Bordon, Yvonne. "Macrophages throw tumour cells a lifeline." Nature Reviews Immunology 19, no. 4 (March 5, 2019): 202–3. http://dx.doi.org/10.1038/s41577-019-0148-1.

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

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Carpenter, Ben, Sara Ghorashian, Emma Nicholson, James Edward Griffin, Maryam Ahmadi, Angelika Holler, Barry Flutter, et al. "Targeting Therapeutic T Cells to Tumour Niches." Blood 120, no. 21 (November 16, 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 targeting therapeutic T cells to CXCR4-dependent niches will improve eradication of tumours in mice. Methods: The murine CXCR4 gene was inserted into retroviral vector, pMP71. Murine T cells were transduced with CXCR4 or control vector and tested for homing in vitro to CXCL12 through chemotaxis assays. In vivo imaging of the putative endosteal bone marrow (BM) niche was performed by multiphoton imaging through cranial frontal bones in osteoblast (collagen 1-α-GFP) reporter mice. In vivo trafficking, competitive transfer and memory recall experiments were performed following transfer of transduced T cells to syngeneic, sub-lethally irradiated mice. Anti-tumour reactivity of CXCR4-transduced T cells was tested in models of allogeneic BM transplantation (BMT). Results: CXCR4-transduced T cells demonstrated enhanced migration towards CXCL12 in vitro. No differences in viability, phenotype or function were observed in CXCR4-transduced versus control T cells in the presence or absence of CXCL12. In competitive assays, CXCR4-transduced CD8 T cells demonstrated a 2-fold greater capacity than controls to home to the BM by 24h after transfer to sub-lethally-irradiated recipients. Multiphoton imaging through cranial frontal bones indicated that fluorescently labelled CXCR4-transduced T cells were closer than control cells to the endosteum (13 μm versus 17 μm, p<0.01). By 14 days, the numbers of CXCR4-transduced CD8 T cells in the BM were 15-fold greater than controls. To test immunity to model antigen, CXCR4 or control vector-transduced OT-1 TCR-transgenic CD8 cells were transferred to sub-lethally irradiated mice before challenge with OVA peptide-loaded dendritic cells. Pre-vaccination, CXCR4-transduced OT-1 cells demonstrated greater engraftment than controls in the BM and spleen. Seven days following vaccination, CXCR4 OT-1 cells demonstrated a greater capacity than control cells to generate IFN-γ to OVA-peptide. Four weeks following vaccination, CXCR4-transduced CD8 T cells showed increased frequencies of cells with a CD44highIL-7Rαhigh memory phenotype than controls, with a greater proportion of cells undergoing proliferation as evaluated by BrdU incorporation. To test T cell immunity against a tumor that exploits the CXCR4-CXCL12 axis to recruit regulatory T cells, B6 BM and CXCR4- or control transduced B6 T cells were transferred to irradiated BALB/c recipients given A20 tumor. Tumor growth was delayed to a greater extent following transfer of CXCR4-compared to control-transduced donor T cells. Conclusion: Over-expression of CXCR4 in CD8 T cells potentiates engraftment, initial effector function and generation of memory cells. Disclosures: Stauss: Cell Medica: Scientific Advisor Other.
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Battke, Christina, Romana Ruiss, Ulrich Welsch, Pauline Wimberger, Stephan Lang, Simon Jochum, and Reinhard Zeidler. "Tumour exosomes inhibit binding of tumour-reactive antibodies to tumour cells and reduce ADCC." Cancer Immunology, Immunotherapy 60, no. 5 (February 4, 2011): 639–48. http://dx.doi.org/10.1007/s00262-011-0979-5.

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Dissertations / Theses on the topic "Immunology; Tumour cells"

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Dearman, Rebecca Jane. "Antibody-dependent destruction of neoplastic cells by celluar effectors." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276345.

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McDonnell, Alison. "The role of dendritic cells in the cross-presentation of tumour antigens." University of Western Australia. School of Medicine and Pharmacology, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0017.

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[Truncated abstract] A paradox exists in tumour immunology whereby progressive tumour growth exists in parallel with an anti-tumour T cell response. This defective T cell response is thought to result from the induction of T cell tolerance and/or tumour induced immunosuppression, which act to inhibit the activation, differentiation and function of tumour-specific CD8+ T cells. Dendritic cells (DCs) are professional antigen presenting cells (APCs) that are critical to the generation of effective CTL; however their function and phenotype is often defective or altered in tumour-bearing hosts, which may limit their capacity to mount an effective tumour specific T cell response. In this thesis, the role of DCs in the cross-presentation of tumour antigen was assessed in terms of their APC function, migration and location. In doing so the intention was to gain insight into the early processes that potentially contribute to the development of an ineffective anti-tumour immune response. This study examined cross-presentation of the nominal tumour antigen, influenza A hemagglutinin (HA) expressed by the murine malignant mesothelioma cell line, AB1-HA. Cross-presentation was predominantly restricted to the local draining lymph nodes throughout tumour growth and was mediated by CD8a+ and CD8a- DCs. This results in an ineffective CTL response due to the lack of DC activation and the presence of potentially immunosuppressive B7 molecules. However, the capacity of the CD8a- DC subset to cross-present antigen suggested a role for migratory tumour-resident DCs in this process. Analysis of tumour infiltrating DCs showed that they were paralysed in their capacity to cross-present tumour antigen and were immobilised at the tumour site. Conversely, cross-presentation of tumour antigen in the local draining lymph node was dependent on the continuous traffic of antigen from the tumour microenvironment. In this vein, small numbers of metastatic tumour cells were detected in the draining lymph nodes, however their isolation was dependent on the removal of DCs and T cells, suggesting immune control of metastatic spread. Thus, tumour cells may be the source of antigen for cross-presentation by DCs in the tumour draining lymph nodes. .... In conclusion, the results presented in this thesis support a role for DCs in the generation of tumour-specific T cell responses that fail to control tumour growth. In addition the results provide a basis for further investigation into the effects of chemotherapy on the source and form of tumour antigen for cross-presentation by specific DC subsets in the tumour bearing host. These findings may have important implications for the development of future anti-cancer immune therapies targeting DCs.
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Ajzensztejn, Daniel. "Harnessing the immune system to reject cancers through genetic modifications of tumour cells." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:1aafa1f4-ee10-4081-b621-d81b9979d96a.

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The immune system, which defends the body against a wide array of threats, is gaining a growing role in the fight against cancer. For an immunotherapy to be successful, it needs to overcome intrinsically weak tumour-specific immune responses. There are two broad approaches to achieving this goal: targeting the various arms of the immune system or targeting the cancer and its microenvironment. The experiments discussed in this thesis adopt the second approach. Tumours were transduced with a combination of costimulatory molecules: CD48, CD54, CD70 & CD86, the chemokine CX3CL1 and the cytokines: IFNγ, GM-CSF and IL-12. Transduction of costimulatory molecules enhances priming in-vitro and cause tumour rejection and delayed tumour growth in-vivo. This effect is demonstrated with single costimulatory molecules but is more pronounced when multiple costimulatory molecules are transduced. Addition of the cytokines and chemokine enhanced tumour rejection, and also resulted in partial rejection of contralateral parental tumours. Attempts to enhance anti-tumour memory by fusing IL-2 and IL-15 to their respective receptors are also discussed. Work in a human/mouse chimeric PD-1 mouse model shows that transduction of multiple costimulatory molecules is able to overcome intrinsic anti-PD-1 resistance. Radiation is known to result in upregulation of several costimulatory molecules within tumours or their infiltrating dendritic cells. The experiments presented here suggest that radiation therapy may be useful in overcoming anti-PD-1 therapy resistance. In human trials, approximately three quarters of cancers fail to respond to anti-PD-1 therapies. Understanding and potentially overcoming anti-PD-1 therapy resistance is therefore of great interest.
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Windebank, Kevin. "Early signal transduction events during activation of the cytolytic process in human natural killer cells." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337563.

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Pullyblank, Anne Maria. "Evaluation of the role of monoclonal antibodies m17-1A, c17-1A and cSF25 in antibody-dependent cell-mediated cytotoxicity and an exploration of the possible mechanisms of action." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268015.

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Petrovic, Kristina. "Exploring the therapeutic potential of CAR-engineered T-cells targeting endothelial markers on tumour and inflamed vasculature." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8468/.

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T-cells engineered to target tumour antigens through surface-expressed chimeric antigen receptors (CARs) are highly effective in treating some leukaemias. The challenge is to extend this success to solid tumours. Tumour endothelial marker 8 (TEM8) is a conserved transmembrane protein overexpressed on the vasculature of many solid tumours but low or undetectable on healthy tissues, making it a potential CAR T -cell target. This thesis explores the safety and therapeutic efficacy of this approach by generating five human TEM8-specific CARs, expressing them in T-lymphocytes, and characterising their functional responses to TEM8 in vitro. Four of the five CARs showed unexpected reactivity to control cells, and in mouse studies some of these proved toxic while most were selectively lost from the circulation, an effect that was TEM8-dependent. Only one CAR selectively responded to target cells overexpressing human TEM8 in vitro but was unable to recognise mouse TEM8, so further in vivo studies were not possible. These results highlight the sensitivity and potency of CAR -engineered T -cells and demonstrate the need for additional safety measures if targeting TEM8. The thesis also demonstrates that another TEM, CLEC14A, is overexpressed in some inflammatory liver diseases, and identifies a suitable mouse model for exploring the therapeutic potential ofCLEC14A-specific CAR-expressing regulatory T-cells.
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Nirmal, Ajit Johnson. "Deconvolution of the immune landscape of cancer transcriptomics data, its relationship to patient survival and tumour subtypes." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31519.

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The immune response to a given cancer can profoundly influence a tumour's trajectory and response to treatment, but the ability to analyse this component of the microenvironment is still limited. To this end, a number of immune marker gene signatures have been reported which were designed to enable the profiling of the immune system from transcriptomics data from tissue and blood samples. Our initial analyses of these resources suggested that these existing signatures had a number of serious deficiencies. In this study, a co-expression based approach led to the development of a new set of immune cell marker gene signatures (ImSig). ImSig supports the quantitative and qualitative assessment of eight immune cell types in expression data generated from either blood or tissue. The utility of ImSig was validated across a wide variety of clinical datasets and compared to published signatures. Evidence is provided for the superiority of ImSig and the utility of network analysis for data deconvolution, demonstrating the ability to monitor changes in immune cell abundance and activation state. ImSig was also used to examine immune infiltration in the context of cancer classification and treatment. Patient-matched ER+ breast cancer samples before and after treatment with letrozole were analysed. Significant elevation of infiltration of macrophages and T cells on treatment was observed in responders but not in non-responders, potentially revealing a biomarker for response. ImSig was also used to study the immune infiltrate in 12 cancer types. By computing the relative abundance of immune cells in these samples, their relationship to survival was investigated. It was interesting to observe that half of the cancers showed trends towards poor prognosis with increased infiltration of immune cells. ImSig alongside the network-based framework can also be used for a more explorative analysis such as to identify biomarkers and activation or differentiation states of immune cells. Melanoma is a highly immunogenic cancer and has shown tremendous success with immune checkpoint inhibitors in a subset of patients. In chapter-6, the molecular subgrouping of melanoma was explored using a network-based approach. Despite the plethora of evidence suggesting various aspects of the immune system to contribute towards the response to immunotherapy in melanoma, there has been little to no effort to consider this heterogeneity while developing molecular subgroups. The use of ImSig was therefore explored for the stratification of melanoma patients into immuno-subgroups. The subgrouping methodology divided the tumours into four groups with different immune profiles. Interestingly, these groupings showed prognostic significance, reiterating the need to consider the heterogeneity of immune cells in future studies. On identifying the most dominant phenotypes that contribute towards prognosis of these patients and in comparison to the published subgroupings of melanoma, we argue that the subgroup of samples enriched in keratin genes are not clinically meaningful. ImSig and the associated analysis framework described in this work, support the retrospective analysis of tissue derived transcriptomics data enabling better characterisation of immune infiltrate associated with disease, and in so doing, provide a resource useful for prognosis and potentially in guiding treatment.
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Chong, Tsung Wen. "Targeting the hypoxic tumour phenotype with specific T-cell immunotherapy." Thesis, University of Oxford, 2004. http://ora.ox.ac.uk/objects/uuid:d22f1d74-44eb-4560-9249-f6127accd1b1.

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Sugiyarto, Gessa. "Characterising the preferential suppression of potent anti-tumour CTL responses by regulatory T cells." Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/379016/.

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Li, Ka-Kit. "The role of CD8+ regulatory T cells in anti-tumour immune responses in hepatocellular carcinoma." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/7940/.

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Tumour specific effector T-cells can be detected in the blood and tumours of patients with hepatocellular carcinoma (HCC) but fail to mount effective immune responses. Attempts to amplify anti-tumour immune responses using immunotherapy show promise, but are hampered by the presence of suppressive regulatory T-cells (Treg) that inhibit anti-tumour immune responses. Many different subsets of Treg have since been identified including regulatory T-cells expressing the surface marker CD8 (CD8⁺Treg). A set of experiments was designed in an attempt to increase our understanding on how CD8⁺Treg may disrupt anti-tumour response and by what mechanisms they are induced. CD8⁺Treg was analysed by isolation of liver-derived T-cells from human HCC. Monocyte-derived dendritic cells (moDC) matured with tumour tissue conditioned medium were used to assess they potential to induce CD8⁺Treg. CD8⁺Treg infiltrating HCC demonstrated a suppressive phenotype. The co-culture of naïve CD8⁺T-cells with tumour-conditioned moDC induces a population of CD8⁺Treg through an IDO dependent mechanism. This population of induced T-cells was able to suppress via the CD39-adenosine pathway. The findings of the mechanisms involved in the induction of CD8⁺Treg by DC and the involvement of CD39 in the suppressive capacity of these novel T-cells, may guide the development of future immunotherapeutic in HCC.
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Books on the topic "Immunology; Tumour cells"

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service), SpringerLink (Online, ed. Natural Killer Cells: At the Forefront of Modern Immunology. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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A, Berzofsky Jay, and SpringerLink (Online service), eds. Natural Killer T cells: Balancing the Regulation of Tumor Immunity. New York, NY: Springer Science+Business Media, LLC, 2012.

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service), SpringerLink (Online, ed. Innate and Adaptive Immunity in the Tumor Microenvironment. Dordrecht: Springer Science + Business Media, LLC, 2008.

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Tumor-infiltrating lymphocytes in human malignancies. Austin: R.G. Landes Co., 1993.

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Alexander, Michael A. Immune-based cancer treatment: The T lymphocyte response. Boca Raton, FL: CRC Press, 2011.

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(Editor), Giorgio Parmiani, and Michael T. Lotze (Editor), eds. Tumor Immunology: Molecularly Defined Antigens and Clinical Applications (Tumor Immunology and Immunotherapy). CRC, 2002.

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Giorgio, Parmiani, and Lotze Michael T, eds. Tumor immunology: Molecularly defined antigens and clinical applications. London: Taylor & Francis, 2002.

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Alexander, Michael A. Functional and Translational Immunology of Regulatory T Cells (Tregs), the Anti-Tumor T Cell Response, and Cancer. Nova Science Publishers, Incorporated, 2014.

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1956-, Stauss Hans J., Kawakami Yutaka, and Parmiani Giorgio, eds. Tumor antigens recognized by T cells and antibodies. London: Taylor & Francis, 2003.

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1956-, Stauss Hans J., Kawakami Yutaka, and Parmiani Giorgio, eds. Tumor antigens recognised by T cells and antibodies. New York, NY: Taylor & Francis, 2003.

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Book chapters on the topic "Immunology; Tumour cells"

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Todryk, Stephen, Selman Ali, Angus Dalgleish, and Robert Rees. "Genetically modified tumour cells for cancer immunization." In Cancer Immunology, 181–94. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-0963-7_11.

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Vánky, F., E. Klein, J. Willems, K. Böök, T. Ivert, and A. Péterffy. "Recognition of Autologous Tumour Cells by Blood Lymphocytes in Patients with Lung Cancer." In Immunology of Malignant Diseases, 105–28. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3219-7_7.

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Onji, Morikazu. "Dendritic Cells in Tumor Immunology." In Dendritic Cells in Clinics, 95–129. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-67011-7_6.

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Wei, Wei-Zen, and Gloria H. Heppner. "Breast cancer immunology." In Mammary Tumor Cell Cycle, Differentiation, and Metastasis, 395–410. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1259-8_19.

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Kim, Chang H. "Regulatory T-Cells and Th17 Cells in Tumor Microenvironment." In Cancer Immunology, 91–106. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30845-2_6.

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Pisapia, David, and Ehud Lavi. "Tumor-Infiltrating T Cells." In Encyclopedia of Medical Immunology, 1230–33. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_10.

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Denton, Alice E., Edward W. Roberts, and Douglas T. Fearon. "Stromal Cells in the Tumor Microenvironment." In Stromal Immunology, 99–114. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78127-3_6.

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Wolf, J., M. Pawlita, J. Bullerdick, and H. zur Hausen. "Tumor Suppression in Somatic Cell Hybrids Between Burkitt’s Lymphoma Cells and EBV-Immortalized Lymphoblastoid Cells." In Progress in Immunology, 502–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_66.

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Gulic, Tamara, Rita Silva-Gomes, Sadaf Davoudian, Marina Sironi, Paola Allavena, Alberto Mantovani, and Barbara Bottazzi. "Tumor-Associated Myeloid Cells in Cancer Progression." In Cancer Immunology, 29–46. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30845-2_3.

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Tavakolpour, Soheil, and Mohammad Darvishi. "The Roles of CD4+ T-Cells in Tumor Immunity." In Cancer Immunology, 63–90. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-30845-2_5.

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Conference papers on the topic "Immunology; Tumour cells"

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Chan, Isaac S., Hildur Knútsdóttir, Gayathri Ramakrishnan, Veena Padmanaban, Manisha Warrier, Juan Carlos Ramirez, Matthew Dunworth, et al. "Abstract PO039: Cancer cells educate natural killer cells to a metastasis-promoting cell state." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po039.

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Xu, Yuexin, Alicia J. Morales, Andrea M. H. Towlerton, Edus H. Warren, and Scott S. Tykodi. "Abstract A36: Single-cell characterization of tumor-infiltrating T cells from renal cell carcinoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a36.

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Aggarwal, Sadhna, Suresh C. Sharma, and Satya N. Das. "Abstract PO082: Significance of Treg cells in pathogenesis of oral squamous cell carcinoma." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po082.

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Sheffer, Michal, Emily Lowry, Nicky Beelen, Minasri Borah, Suha Naffar-Abu Amara, Chris C. Mader, Jennifer Roth, et al. "Abstract PO041: Landscape of molecular events regulating tumor cell responses to natural killer cells." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po041.

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Kristensen, Nikolaj Pagh, Christina Heeke, Siri A. Tvingsholm, Anne-Mette Bjerregaard, Arianna Draghi, Amalie Kai Bentzen, Rikke Andersen, Marco Donia, Inge Marie Svane, and Sine Reker Hadrup. "Abstract A14: Neoepitope-specific CD8+ T cells in adoptive T-cell transfer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a14.

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Cassereau, Luke, Tia DiTommaso, Scott Loughhead, Jonathan Gilbert, Howard Bernstein, and Armon Sharei. "Abstract A55: Vector-free genome editing of immune cells for cell therapy." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a55.

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Gordon, Stuart, Bonnie Sloane, Phil Cavanugh, Barbara Cross, Kenneth Honn, and Mohanathasan Chelladurai. "PURIFICATION AND CHARACTERIZATION OF TWO PROCOAGULANTS FROM WALKER 256 CARCINOSARCOMA TUMORS,." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643666.

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Abstract:
Activation of the coagulation system bytumor cells may play an important role in tumor growth and metastases. Becauseprocoagulant activities have been identified in different tumor cells by different investigators, effective comparison of these activities has been difficult. Therefore, we purified and characterized two different procoagulant proteins from the same Walker 256 tumors. The first procoagulant activity/platelet aggregating activity (PCA/PAA) was purified from a 1% CHAPS detergent extract oftumor homogenate followed by (NH4)2SO4 fractionation, anion exchange and hydrophobic chromatography. The protein had a molecular weight of 58,000, required phospholipid and an intact coagulation pathway from factor X through fibrinogen for activity, but did not require factors VII or IX forits procoagulant activity. The procoagulant activity was not inhibited by 5mMphenyl-methyl sulfonyl fluoride, iodoacetamide or phenanthroline; there was noevidence of proteinase activity. The PAA was due to thrombin generation during coagulation. The second procoagulant,cancer procoagulant (CP), was extracted from tumors in barbital buffer (pH 7.4) without detergent, purified by immunoaffinity (using a polyclonal goat antibody to CP from V2 carcinoma) and mercurial-benzoate affinity chromatography. CP had a molecular weight of 68,000, an isoelectric point of 4.8 and initiated coagulation by directly activating factor X in the coagulation system. CP was inhibited by Hg++ and iodoacetamide, cysteine proteinase inhibitors. The purified CP formed an immunodiffusion precipitin band against the polyclonal anti-CP goat antibody. Thus, thepurified CP had the same physicochemical, enzymatic and immunologic propertiesas CP from rabbit V2 carcinoma. Neither procoagulant had the properties of tissue factor. These results suggest that there aretwo distinct procoagulant activities inWalker 256 and that both may contributeto the coagulation abnormalities that are associated with tumor growthand metastases.
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Mukherjee, Debarati, Robert Baldi, Ching-Yi Chang, Luigi Racioppi, and Donald P. McDonnell. "Abstract A51: Impact of CaMKK2 inhibition in tumor-associated myeloid cells on CD8+ cytotoxic T-cell recruitment into mammary tumors." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a51.

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Pauken, Kristen E., Osmaan Shahid, Kaitlyn A. Lagattuta, Kelly M. Mahuron, Jacob M. Luber, Margaret M. Lowe, Linglin Huang, et al. "Abstract PO016: Single-cell analyses characterize circulating anti-tumor CD8 T cells and identify markers for their isolation." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po016.

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Ma, Liqian, Lawrence Wang, Adam T. Nelson, Chaeyeon Han, Sisi He, Madeline A. Henn, Karan Menon, et al. "Abstract PR006: 27-Hydroxycholesterol acts on myeloid immune cells to induce T cell dysfunction, promoting breast cancer progression." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-pr006.

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