Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors
Emphasizing the dynamic processes between cancer and host immune system, the initially discovered concept of cancer immunosurveillance has been replaced by the current concept of cancer immunoediting consisting of three phases: elimination, equilibrium, a
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Cancer Immunoediting: Elimination, Equilibrium, and Immune Escape in Solid Tumors Jacek R. Wilczynski and Marek Nowak
Abstract Emphasizing the dynamic processes between cancer and host immune system, the initially discovered concept of cancer immunosurveillance has been replaced by the current concept of cancer immunoediting consisting of three phases: elimination, equilibrium, and escape. Solid tumors composed of both cancer and host stromal cells are an example of how the three phases of cancer immunoediting functionally evolve, and how a tumor shaped by the host immune system gets a finally resistant phenotype. Elimination, equilibrium, and escape are described in this chapter in detail, including the role of immune surveillance, cancer dormancy, disruption of the antigen-presenting machinery, tumor-infiltrating immune cells, and resistance to apoptosis, as well as the function of tumor stroma, microvesicles, exosomes and inflammation.
List of Abbreviations AFP APCs APM CAFs CCR7 CEA
Alpha-fetoprotein Antigen-presenting cells Antigen-processing machinery Cancer-associated fibroblasts C–C chemokine receptor type 7 Carcinoembryonic antigen
J.R. Wilczynski (*) Department of Gynecology, Polish Mother’s Memorial Hospital – Research Institute, Lodz, Poland Medical University of Lodz, Lodz, Poland e-mail: [email protected] M. Nowak Department of Gynecology and Gynecologic Oncology, Polish Mother’s Memorial Hospital – Research Institute, Lodz, Poland M. Klink (ed.), Interaction of Immune and Cancer Cells, DOI 10.1007/978-3-7091-1300-4_8, © Springer-Verlag Wien 2014
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COX CSCs CSF-1 CTLA-4 CTLs CXCR1 DCs DTCs ECM EGF EMT EOC FasL FGF GITR GLI GM-CSF Hh HIF-1α HLA HPV Hsp IAPs ICAM-1 IDO IFN IGF IL ILT JAK JNK MAPK M-CSF MDSCs MMPs MVD NF-κB NK NKG2D NKT NO PBLs PD-1 PDGF PGE2
J.R. Wilczynski and M. Nowak
Cyclooxygenase Cancer stem cells Colony-stimulating factor-1 Cytotoxic T-lymphocyte antigen 4 Cytotoxic T lymphocytes Interleukin 8 receptor, alpha Dendritic cells Disseminated solitary tumor cells Extracellular matrix Epidermal growth factor Epithelial–mesenchymal transition or transformation Epithelial ovarian cancer Fas ligand Fibroblast growth factor Glucocorticoid-induced tumor necrosis factor receptor Glioma-associated oncogene homolog Granulocyte–macrophage colony-stimulating factor Hedgehog signaling Hypoxia-inducible factor-1α Human leukocyte antigen Human papilloma virus Heat-shock protein Inhibitor of apoptosis proteins Intercellular adhesion molecule 1 Indoleamine 2,3-dioxygenase Interferon Insulin-like growth factor Interleukin Immunoglobulin-like transcript Janus kinase c-Jun N-terminal kinases Mitogen-activated protein kinases Macrophage colony-stimulating factor Myeloid-derived suppressor cells Metalloproteinases Microvessel density Nuclear factor-κB Natural killer cells Activating receptor of NK cells Natural killer T cells nitric oxide Peripheral blood lymphocytes Programmed death-1 and its ligand PD-L1 (also called B7-H1) Platelet-derived growth factor Prostaglandin E2
8 Cancer Immunoedit
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