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Author: Maryse Dagenais Publisher: ISBN: Category : Languages : en Pages :
Book Description
"Innate immunity is the host's first line of defense. Among its physiological mechanisms is the induction of cell death and inflammation, which rid the host of infectious and non-infectious insults and restore tissue homeostasis. Although beneficial, these responses are deleterious, if unchecked, contributing to inflammatory pathologies and diseases of homeostasis such as cancer. Several checkpoints regulate the extent of inflammation and cell death, including the inhibitor of apoptosis proteins (IAPs), the inflammasomes and Interleukin (IL)-1 receptor signaling. Notably, genetic perturbations of these factors are associated with inflammatory diseases and cancer. To investigate the role of the cellular IAP (cIAP)s in tissue homeostasis and cancer, we explored the impact of cIAP2 gene deletion in mice (Birc3-/- mice) on colitis and colitis-associated colorectal cancer (CAC). We identified that cIAP2 acted as a driver of CAC but was required for intestinal tissue repair following injury by mediating inflammasome signaling and inhibiting apoptosis. To further investigate the functions of the cIAPs in the small intestine, we assessed the response of Birc3-/- mice to infection with murine norovirus (MNV). This infection elicits endoplasmic reticulum (ER) stress in the highly secretory Paneth cells and results in an aberrant granule packaging when this stress is unresolved. Our results identified cIAP1 and cIAP2 as proximal mediators of the unfolded protein response (UPR) in intestinal epithelial cells, specifically in response to MNV infection and aberrant protein glycosylation. To examine the role of innate immunity in tumorigenesis at a relatively sterile site, we interrogated the role of the inflammasome and IL-1R signaling in an animal model of spontaneous breast cancer and lung metastasis driven by the oncogene PyMT. We found that IL-1R1 signaling was a negative regulator of PyMT-mediated mammary tumors. We provided evidence that this phenotype was, at least in part, dependent on IL-1, but independent of the caspase-1 inflammasome pathway. Collectively, this thesis presents novel findings on the role of innate immunity effectors in the pathogenesis of inflammatory bowel disease (IBD) and cancer (CAC and breast cancer) and advances new therapeutic avenues for the treatment of these illnesses. " --
Author: Maryse Dagenais Publisher: ISBN: Category : Languages : en Pages :
Book Description
"Innate immunity is the host's first line of defense. Among its physiological mechanisms is the induction of cell death and inflammation, which rid the host of infectious and non-infectious insults and restore tissue homeostasis. Although beneficial, these responses are deleterious, if unchecked, contributing to inflammatory pathologies and diseases of homeostasis such as cancer. Several checkpoints regulate the extent of inflammation and cell death, including the inhibitor of apoptosis proteins (IAPs), the inflammasomes and Interleukin (IL)-1 receptor signaling. Notably, genetic perturbations of these factors are associated with inflammatory diseases and cancer. To investigate the role of the cellular IAP (cIAP)s in tissue homeostasis and cancer, we explored the impact of cIAP2 gene deletion in mice (Birc3-/- mice) on colitis and colitis-associated colorectal cancer (CAC). We identified that cIAP2 acted as a driver of CAC but was required for intestinal tissue repair following injury by mediating inflammasome signaling and inhibiting apoptosis. To further investigate the functions of the cIAPs in the small intestine, we assessed the response of Birc3-/- mice to infection with murine norovirus (MNV). This infection elicits endoplasmic reticulum (ER) stress in the highly secretory Paneth cells and results in an aberrant granule packaging when this stress is unresolved. Our results identified cIAP1 and cIAP2 as proximal mediators of the unfolded protein response (UPR) in intestinal epithelial cells, specifically in response to MNV infection and aberrant protein glycosylation. To examine the role of innate immunity in tumorigenesis at a relatively sterile site, we interrogated the role of the inflammasome and IL-1R signaling in an animal model of spontaneous breast cancer and lung metastasis driven by the oncogene PyMT. We found that IL-1R1 signaling was a negative regulator of PyMT-mediated mammary tumors. We provided evidence that this phenotype was, at least in part, dependent on IL-1, but independent of the caspase-1 inflammasome pathway. Collectively, this thesis presents novel findings on the role of innate immunity effectors in the pathogenesis of inflammatory bowel disease (IBD) and cancer (CAC and breast cancer) and advances new therapeutic avenues for the treatment of these illnesses. " --
Author: Bharat B. Aggarwal Publisher: Springer ISBN: 3034808372 Category : Medical Languages : en Pages : 489
Book Description
This volume examines in detail the role of chronic inflammatory processes in the development of several types of cancer. Leading experts describe the latest results of molecular and cellular research on infection, cancer-related inflammation and tumorigenesis. Further, the clinical significance of these findings in preventing cancer progression and approaches to treating the diseases are discussed. Individual chapters cover cancer of the lung, colon, breast, brain, head and neck, pancreas, prostate, bladder, kidney, liver, cervix and skin as well as gastric cancer, sarcoma, lymphoma, leukemia and multiple myeloma.
Author: Wen Zhou Publisher: ISBN: Category : Languages : en Pages :
Book Description
Cell death and innate immunity are interconnected events for multicellular organisms to defend against pathogenic microbes and restrict tissue damage. Macrophages constitute an important population of innate immunity. Their survival and activation are critical for the local and systematic inflammation. Tumor necrosis factor (TNF) is an important pro-inflammatory factor and a major cause of cell death in vivo under pathological conditions. TNF can promote apoptosis, a hypoimmunogenic type of cell death that is preferentially triggered to restrict inflammation, or necroptosis, an immunogenic type of cell death that releases danger signals to the environment. These danger signals activate immune receptors such as toll-like receptors (TLRs). TLRs are the major family of receptors that sense extracellular pathogen- or damage-associated molecular patterns and elicit pro-inflammatory or antiviral responses.
Author: Han-Ming Shen Publisher: Springer Science & Business Media ISBN: 1461482208 Category : Science Languages : en Pages : 402
Book Description
Starting with discussion of basic concepts and the molecular mechanisms of necrosis, this book looks first at several forms of necrotic cell death that have been identified, including necroptosis, autophagic cell death, and PARP-mediated cell death. As necrotic cell death is increasingly known to play a critical role in many physiological processes, the next chapters discuss its effect on metabolism, inflammation, immunity, and development. Necrotic cell death is closely implicated in human diseases like cancer, so the next chapters examine its relevance to human diseases, and final chapters cover methodologies for measuring necrosis. This book presents comprehensive coverage of necrosis from recognized experts from leading academic and medical institutions around the world. In contrast to apoptosis, well-defined as a form of programmed cell death, necrosis used to be considered as accidental (i.e., non-programmed) cell death, usually in response to a severe injury. Accumulating evidence now suggests, however, that necrosis is also programmed and controlled by distinctive "death machinery" in response to various stimuli like oxidative stress or DNA damage.
Author: Laurence Zitvogel Publisher: Springer ISBN: 3319624318 Category : Medical Languages : en Pages : 700
Book Description
In this book, leading experts in cancer immunotherapy join forces to provide a comprehensive guide that sets out the main principles of oncoimmunology and examines the latest advances and their implications for clinical practice, focusing in particular on drugs with FDA/EMA approvals and breakthrough status. The aim is to deliver a landmark educational tool that will serve as the definitive reference for MD and PhD students while also meeting the needs of established researchers and healthcare professionals. Immunotherapy-based approaches are now inducing long-lasting clinical responses across multiple histological types of neoplasia, in previously difficult-to-treat metastatic cancers. The future challenges for oncologists are to understand and exploit the cellular and molecular components of complex immune networks, to optimize combinatorial regimens, to avoid immune-related side effects, and to plan immunomonitoring studies for biomarker discovery. The editors hope that this book will guide future and established health professionals toward the effective application of cancer immunology and immunotherapy and contribute significantly to further progress in the field.
Author: David A. Frank Publisher: Springer Science & Business Media ISBN: 1402073402 Category : Medical Languages : en Pages : 358
Book Description
One of the most exciting areas of cancer research now is the development of agents which can target signal transduction pathways that are activated inappropriately in malignant cells. The understanding of the molecular abnormalities which distinguish malignant cells from their normal counterparts has grown tremendously. This volume summarizes the current research on the role that signal transduction pathways play in the pathogenesis of cancer and how this knowledge may be used to develop the next generation of more effective and less toxic anticancer agents. Series Editor comments: "The biologic behavior of both normal and cancer cells is determined by critical signal transduction pathways. This text provides a comprehensive review of the field. Leading investigators discuss key molecules that may prove to be important diagnostic and/or therapeutic targets."
Author: Geeta Rai Publisher: Academic Press ISBN: 0128163798 Category : Medical Languages : en Pages : 200
Book Description
NETosis: Immunity, Pathogenesis and Therapeutics takes a focused approach to the clinical aspects of NETosis and drug development, bringing critical findings. Chapters introduce NETosis, consider mechanisms and antimicrobial strategies regulating NETosis, examine NETosis in neonates, explore the role of NETosis in autoimmunity, delve into NETosis and other diseases, and present therapeutic approaches for dysregulated NETosis. Since Brinkamm, et al, discovered an unrecognized neutrophil anti-microbial mechanism responsible for the extracellular killing of invading pathogens in 2004, the novel process in which nuclear chromatin de-condenses and DNA is ejected into the extra cellular environment, trapping and inactivating tissue pathogens has rapidly evolved. Presents an up-to-date and detailed analysis of NETosis Brings together critical findings on NETosis as a comparatively novel immune mechanism Focuses on the clinical aspects of NETosis that lead to drug development Covers the topic with a cogency and passion that is based on years of scientific research
Author: Patrizia Agostinis Publisher: Springer Science & Business Media ISBN: 9400743513 Category : Medical Languages : en Pages : 448
Book Description
The Endoplasmic Reticulum (ER) is an organelle with extraordinary signaling and homeostatic functions. It is the organelle responsible for protein folding, maturation, quality control and trafficking of proteins destined for the plasma membrane or for secretion into the extracellular environment. Failure, overloading or malfunctioning of any of the signaling or quality control mechanisms occurring in the ER may provoke a stress condition known as ‘ER stress’. Accumulating evidence indicates that ER stress may dramatically perturb interactions between the cell and its environment, and contribute to the development of human diseases, ranging from metabolic diseases and cancer to neurodegenerative diseases, or impact therapeutic outcome. This book primarily focuses on the pathophysiology of ER stress. It introduces the molecular bases of ER stress, the emerging relevance of the ER-mitochondria cross-talk, the signaling pathways engaged and cellular responses to ER stress, including the adaptive Unfolded Protein Response (UPR), autophagy as well as cell death. Next the book addresses the role of ER stress in physiology and in the etiology of relevant pathological conditions, like carcinogenesis and inflammation, neurodegeneration and metabolic disease. The last chapter describes how ER stress pathways can be targeted for therapeutic benefit. Altogether, this book will provide the reader with an exhaustive view of ER stress biology and the latest insights in the role of ER stress in relevant human diseases.
Author: Stuart K. Calderwood Publisher: Springer Science & Business Media ISBN: 1402064012 Category : Medical Languages : en Pages : 399
Book Description
Heat shock proteins are emerging as important molecules in the development of cancer and as key targets in cancer therapy. These proteins enhance the growth of cancer cells and protect tumors from treatments such as drugs or surgery. However, new drugs have recently been developed particularly those targeting heat shock protein 90. As heat shock protein 90 functions to stabilize many of the oncogenes and growth promoting proteins in cancer cells, such drugs have broad specificity in many types of cancer cell and offer the possibility of evading the development of resistance through point mutation or use of compensatory pathways. Heat shock proteins have a further property that makes them tempting targets in cancer immunotherapy. These proteins have the ability to induce an inflammatory response when released in tumors and to carry tumor antigens to antigen presenting cells. They have thus become important components of anticancer vaccines. Overall, heat shock proteins are important new targets in molecular cancer therapy and can be approached in a number of contrasting approaches to therapy.
Author: Publisher: Academic Press ISBN: 0128241594 Category : Medical Languages : en Pages : 384
Book Description
Advances in Cancer Research, Volume 150, the latest release in this ongoing series, covers the relationship(s) between autophagy and senescence, how they are defined, and the influence of these cellular responses on tumor dormancy and disease recurrence. Specific sections in this new release include Autophagy and senescence, converging roles in pathophysiology, Cellular senescence and tumor promotion: role of the unfolded protein response, autophagy and senescence in cancer stem cells, Targeting the stress support network regulated by autophagy and senescence for cancer treatment, Autophagy and PTEN in DNA damage-induced senescence, mTOR as a senescence manipulation target: A forked road, and more. Addresses the relationship between autophagy and senescence in cancer therapy Covers autophagy and senescence in tumor dormancy Explores autophagy and senescence in disease recurrence
Author: Maryse Dagenais
Author: Maryse Dagenais
Author: Bharat B. Aggarwal
Author: Wen Zhou
Author: Han-Ming Shen
Author: Laurence Zitvogel
Author: David A. Frank
Author: Geeta Rai
Author: Patrizia Agostinis
Author: Stuart K. Calderwood
Author: