Immune escape is a key mechanism of cancer progression and metastatic dissemination and creates a serious obstacle to successful cancer treatment. It has been widely recognized, indeed, that cancerous cells are capable of escaping immune surveillance and antitumor immunity. There are several factors that contribute to tumor persistence despite a normal host immune system, including intrinsic mechanisms of carcinogenesis or extrinsic immunosuppressive characteristics of the tumor microenvironment. These factors promote immune selection of aggressive tumor cell variants and generate tumor heterogeneity and metastasis, which play a critical role in tumor growth and resistance to immunotherapy. Tumor cells can escape T cells responses by a variety of mechanisms including the loss of the antigen presentation capacity. One of the key mechanisms of tumor rejection is the induction of anti-tumor T-cell mediated cytotoxicity which, in turn, depends on the tumor antigen presentation to T-cells via MHC class I complex.
Thanks to the successful clinical use of monoclonal antibodies targeting molecules involved in the regulation of T cell cytotoxicity, cancer immunotherapy is gaining major clinical interest. New therapies with immune-checkpoint inhibitors unleash anti-tumor immunity and induce regression of metastatic lesions in a large number of cancer patients. However, a substantial proportion of patients show resistance to immunotherapies. It is becoming more and more evident that inducing a strong and long-lasting immune response capable of targeting primary or disseminated cancer cells requires not only the activation of T cells, but also depends on the optimal expression of MHC molecules, the choice of antigen against which immunity has to be triggered, and the mutation rate of the tumor antigens. In the light of these evidences a more in-depth understanding on the mechanism of cancer immune escape is required.
The aim of this Research Topic is to provide a comprehensive overview of our current knowledge of the basis of cancer immune evasion that promotes cancer progression and interferes with cancer immunotherapies. We welcome contributions of Original Research and Review articles on the following mechanisms of cancer escape:
• Innate and acquired resistance to immunotherapy
• Immune selection
• MHC class-I loss in tumor cells
• Tumor dormancy and immune response
• Immune escape in lung cancer, bladder cancer, melanoma and in MSI-colorectal cancer
• Detection of tumor HLA class I alteration in exosomes
• NK cells role in tumour escape
• Cancer-associated fibroblasts (CAFs) and immunosuppression within the tumor microenvironment.
• Cancer immune escape and immunoediting during tumor progression in patients receiving cancer immunotherapy
Immune escape is a key mechanism of cancer progression and metastatic dissemination and creates a serious obstacle to successful cancer treatment. It has been widely recognized, indeed, that cancerous cells are capable of escaping immune surveillance and antitumor immunity. There are several factors that contribute to tumor persistence despite a normal host immune system, including intrinsic mechanisms of carcinogenesis or extrinsic immunosuppressive characteristics of the tumor microenvironment. These factors promote immune selection of aggressive tumor cell variants and generate tumor heterogeneity and metastasis, which play a critical role in tumor growth and resistance to immunotherapy. Tumor cells can escape T cells responses by a variety of mechanisms including the loss of the antigen presentation capacity. One of the key mechanisms of tumor rejection is the induction of anti-tumor T-cell mediated cytotoxicity which, in turn, depends on the tumor antigen presentation to T-cells via MHC class I complex.
Thanks to the successful clinical use of monoclonal antibodies targeting molecules involved in the regulation of T cell cytotoxicity, cancer immunotherapy is gaining major clinical interest. New therapies with immune-checkpoint inhibitors unleash anti-tumor immunity and induce regression of metastatic lesions in a large number of cancer patients. However, a substantial proportion of patients show resistance to immunotherapies. It is becoming more and more evident that inducing a strong and long-lasting immune response capable of targeting primary or disseminated cancer cells requires not only the activation of T cells, but also depends on the optimal expression of MHC molecules, the choice of antigen against which immunity has to be triggered, and the mutation rate of the tumor antigens. In the light of these evidences a more in-depth understanding on the mechanism of cancer immune escape is required.
The aim of this Research Topic is to provide a comprehensive overview of our current knowledge of the basis of cancer immune evasion that promotes cancer progression and interferes with cancer immunotherapies. We welcome contributions of Original Research and Review articles on the following mechanisms of cancer escape:
• Innate and acquired resistance to immunotherapy
• Immune selection
• MHC class-I loss in tumor cells
• Tumor dormancy and immune response
• Immune escape in lung cancer, bladder cancer, melanoma and in MSI-colorectal cancer
• Detection of tumor HLA class I alteration in exosomes
• NK cells role in tumour escape
• Cancer-associated fibroblasts (CAFs) and immunosuppression within the tumor microenvironment.
• Cancer immune escape and immunoediting during tumor progression in patients receiving cancer immunotherapy
