China
Africa
Explore chapters and articles related to this topic
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.
Tumor immunology
Published in Gabriel Virella, Medical Immunology, 2019
It is now well understood that the immune system is not only able to survey and control neoplastic processes, but that by applying this immune pressure it also transforms the tumor and its microenvironment. Cancer immunoediting is the general process by which tumor cells “edit” themselves and/or their microenvironment in response to an antitumor immune response leading to cancer progression. Immune selection leads to the generation of tumor escape variants, and there are multiple mechanisms that lead to the immune evasion by tumors as outlined in Figure 26.2.
Cancer Immunology
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Osama Al Hamarneh, John Greenman
The discovery and identification of tumour antigens has helped scientists begin to understand the key steps in an anti-tumour immune response. In animal models, the encounter between the immune system and tumours initiates a process termed ‘immunoediting’.70 This process can bring about three outcomes: elimination of the tumour; tumour equilibrium, in which there is immune selection of less immunogenic tumours during an anti-tumour immune response;71 and tumour escape, the growth of tumour variants that resist immune destruction.
Tumor spread or siege immunity: dissemination to distant metastasis or not
Published in OncoImmunology, 2021
Gabriela Bindea, Bernhard Mlecnik, Jérôme Galon
The heterogeneous metastatic landscape, described as the number and size of metastatic lesions, their mutational pattern as well as their immune cell infiltrate, evolves under the immune pressure that sculpts the evolution of its clones. During metastatic progression, the immunoedited clones are eliminated, while the immune privileged clones persist and progress underlining relationships between clonal seeding and immune surveillance. The immunoediting score was associated with an active immune response, implying a predictive potential for immunotherapy. Based on the evolvogram, we have proposed a tumor clone development model, called parallel immune selection model, that, in contrast with existing tumor-cell centric models, is linked to the intra-metastatic immune microenvironment via the immunoediting process (Figure 1).8
CD80 expression promotes immune surveillance in Barrett’s metaplasia
Published in OncoImmunology, 2019
Melania Scarpa, Matteo Fassan, Andromachi Kotsafti, Stefano Realdon, Luigi Dall’Olmo, Tiziana Morbin, Francesco Cavallin, Luca Saadeh, Matteo Cagol, Rita Alfieri, Carlo Castoro, Massimo Rugge, Ignazio Castagliuolo, Marco Scarpa
The immune system can specifically identify and eliminate tumor cells on the basis of their expression of tumor-specific antigens or molecules induced by cellular stress.9,10 In this process, known as tumor immune surveillance or immunoediting, the immune system identifies cancerous and/or precancerous cells and eliminates them before they can cause harm. A successful elimination depends on an adequate T-cell priming and proper execution of the effector phase of the immune response. In each of these contexts, a potential role of T-cell costimulatory receptors has been implicated.11 The lack of positive costimulatory ligands such as CD80 has been suggested to contribute to poor anti-tumor T-cell efficacy. Indeed, we have recently demonstrated that in colonic inflammatory carcinogenesis the progression from dysplasia to invasive cancer is controlled by an effective immune surveillance mechanism mediated by CD80 expression on epithelial cells that can completely clear preneoplastic lesions in a large proportion of cases.12
Neoantigen characteristics in the context of the complete predicted MHC class I self-immunopeptidome
Published in OncoImmunology, 2019
Scott D. Brown, Robert A. Holt
Immunoediting is a well accepted phenomenon that occurs during cancer development.31 By comparing observed mutations from immune-exposed TCGA tumors to in silico generated mutations, we were able to detect signals of immune-evasion within the TCGA data. It is important to note that our in silico mutations are random and do not necessarily confer the same cancer growth advantage, or in fact any biological relevance, that is likely found in the set of TCGA mutations and thus are used as a measure of baseline pMHC generation. Compared to in silico mutations, we observed a general trend of decreased immunogenicity for expressed TCGA mutations, and an increase for non-expressed mutations. This supports the view that the majority of TCGA tumors are immune-edited, as we see higher immunogenicity from non-expressed SNVs than would be expected by chance. This could be the result of immune-editing over time shaping the mutational profile of these cancer cells through accumulation of mutations that would be potentially immunogenic if expressed, but are immunologically inconsequential when present in non-expressed genes. Under this framework, we also identified samples that showed evidence of a suppressed immune response, permitting relatively more immunogenic mutations in expressed genes. These subjects demonstrate decreased progression free survival, supporting the concept that these individuals harbour tumours which have suppressed the natural immune response to the tumor.