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Role of Nanoparticles in Cancer Immunotherapy
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
The concept of tumor immune surveillance, i.e., the ability of immune cells to detect and kill the nascent tumor cells, was first of all proposed independently by M.F. Burnet and L. Thomas in 1950s [9, 10]. The idea of cancer immunosurveillance laid the foundation of tumor immunology and cancer immunotherapy. In later years, many clinical and animal studies supported the hypothesis of tumor immunosurveillance. For example, immunodeficient animals show high rate of tumor incidence and this trend is seen in immunodeficient human patients as well. However, immunosurveillance hypothesis could not clarify why the tumor cells still grow despite the ability of immune cells to recognize and eliminate them. To explain this observation, a more inclusive and updated hypothesis was proposed by Dr. Robert Schrieber in 2002, which is popularly known as ‘cancer immunoediting’ [11, 12] (Figure 12.1). The cancer immunoediting hypothesis incorporates both the aspects of immune system, namely, immunoprotective and immunoselective role. The immune system not only protects the host, but can also shape the immunogenicity of tumor. Cancer immunoediting encompasses in three stages defined by the three “Es” namely ‘Elimination (equivalent to immune surveillance)’, ‘Equilibrium’, and ‘Escape’. Cancer cells evade the immune responses by employing or pirating the different immune suppression mechanism that were used to prevent overactivation of immune cells during immune homeostasis.
Tumour Microenvironment Studies in Immuno-Oncology Research
Published in Inna Kuperstein, Emmanuel Barillot, Computational Systems Biology Approaches in Cancer Research, 2019
Inna Kuperstein, Emmanuel Barillot
To comprehensively reveal the contribution of the immune system in this process, the immune landscape of each lesion was evaluated qualitatively, quantitatively and spatially by the means of single-plex IHC staining, digital quantification and multispectral imaging for several immune markers of major lymphocytic lineages, including CD3+, CD8+, FoxP3+ and CD20+; Ki67+ (a cellular marker for proliferation) and cytokeratin (for epithelial cells) were also included in the multiplex analysis. This approach also enabled calculation of the Immunoscore associated to each metastasis/tumour. Plotting the Immunoscore values (High vs Low, henceforth displayed as Hi/Lo) against the corresponding immunoediting score (Yes/No) for each metastatic sample generated four categories: HiYes, HiNo, LoYes and LoNo. No metastasis fell within the LoYes group, reinforcing the hypothesis that T cells are required for immunoediting to occur. Accordingly, the majority of metastases fell in the LoNo category. 54% of the metastases with high Immunoscore were immunoedited. Overall, these results provide the first direct evidence of immunoediting in humans at the metastatic stage, and indicate that T cell infiltration is necessary but not sufficient for immunoediting to occur. When analysing recurrence amongst these four categories, the LoNo were found to produce at least one child metastasis (64% of cases), whilst that was the case for only 8% of the high Immunoscore metastases.
Dosimetry in Electroporation-Based Technologies and Treatments
Published in Marko Markov, Dosimetry in Bioelectromagnetics, 2017
Eva Pirc, Matej Reberšek, Damijan Miklavčič
Gene electrotransfer is a promising non-viral gene delivery method (Kandušer et al., 2009). It is used for treatment of cancer and other diseases (Shibata et al., 2006; Daud et al., 2008), for DNA vaccination (Chiarella et al., 2010; Sardesai and Weiner, 2011), and genetic modification of organisms (Golden et al., 2007; Grewal et al., 2009). “Cancer immunoediting” is a process combining the immune system and tumors. The immune system can protect the host against tumor growth, or promote cancer development by selection of tumor variants with reduced immunogenicity (Zou et al., 2005). Immunotherapy can include cancer vaccines based on plasmid DNA (pDNA) vectors (Serša et al., 2015). Electroporation is used to promote antigen, oligonucleotides, and immunomodulatory molecule delivery in to tumor tissue. They can stimulate the immune system or act on immunosuppressor genes (Serša et al., 2015). In vitro electric pulses are frequently used for the transfection of bacterial and eukaryotic cells. In vivo the technique is termed DNA electrotransfer, electrogenetherapy, or also gene electrotherapy. It has been successfully used since 1998. However, exact molecular mechanisms of DNA transport are unknown (Kandušer et al., 2009; Serša et al., 2015). DNA transfer can only be achieved by reversible electroporation, because dead cells are not able to express transferred genes (Andre et al., 2010). The DNA must be injected before electroporation; the application requires sufficiently intense electric fields, which means sufficiently long pulses should be applied, but we also need to ensure reversible electroporation. Permeabalized cell membrane should interact with the plasmid; thus a DNA–membrane complex is formed. DNA, then, with an as yet unknown process, is transferred into the cytoplasm and transported to the nucleus. In cases where the application is successful, the process is followed by gene expression (Golzio et al., 2002; Faurie et al., 2010).
Modelling tumour–immune dynamics, disease progression and treatment
Published in Letters in Biomathematics, 2018
Amina Eladdadi, Lisette de Pillis, Peter Kim
Both helper T and cytotoxic T cells play a crucial role in the anti-tumour–immune response. How the anti-tumour–immune response varies with the level of infiltrating helper and cytotoxic T cells is the focus of the paper ‘A mathematical model of cytotoxic and helper T cell interactions in a tumour microenvironment’ by H. Dritschel, S.L. Waters, A. Roller and H.M. Byrne. The authors address the heterogeneity of subpopulations of helper and cytotoxic T cells in an anti-tumour immune response by proposing a simple and elegant, yet highly predictive, model consisting of three ordinary differential equations for tumour cells, helper and cytotoxic T cells. Immunosuppressive effects are implicitly included through a biphasic helper T cell proliferation term. The model exhibits the three Es of Immunoediting – elimination, equilibrium and escape. A comprehensive analytical and numerical investigation show that infiltration of both helper and cytotoxic T cells control the conditions for tumour elimination. Moreover, the results suggest that combined therapies which both block immunosuppressive effects and boost the helper and cytotoxic T cell populations may produce the most favourable outcomes.
A mathematical model of cytotoxic and helper T cell interactions in a tumour microenvironment
Published in Letters in Biomathematics, 2018
Heidi Dritschel, Sarah L. Waters, Andreas Roller, Helen M. Byrne
We have proposed a new mathematical model of tumour-immune interactions in which helper and cytotoxic T cells interact with tumour cells. Our model captures the three Es of immunoediting — elimination, equilibrium and escape (Dunn et al., 2004). We have examined how the number and nature of the attractors (stable steady states and limit cycles) change as the infiltration rates of cytotoxic and helper T cells, and , are varied. Our focus on and is motivated by experimental observations which show high inter-patient variability in T cell infiltration rates and corresponding variability in observed outcomes (Oelkrug and Ramage, 2014; Fridman et al., 2012; Halama et al., 2011; Ali et al., 2016). Specifically, high levels of tumour infiltrating T cells have been correlated with long-term progression free survival in a variety of different cancer types (Rad et al., 2015); preston2013ratios; hiraoka2006concurrent.