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This Research Topic is the second volume of the “Community Series in the Role of Angiogenesis and Immune Response in Tumor Microenvironment of Solid Tumor". Please Volume I here. The microenvironment of tumors is consisted of the tumor stroma, proliferating tumor cells, infiltrating inflammatory cells, blood vessels, and various associated tissue cells. The pre-metastatic niche (PRN) is described as supportive and receptive, which undergoes cellular and molecular changes to form the fertile “soil” or metastatic-designated sites for metastatic tumor cell “seed” colonization. Thus, the PRN supports promoting tumor metastasis and tumor settlement in distant organs. The infiltration of the immune cells and the formation of blood vessels from the pre-metastatic sites are critical for the tumor microenvironment. Typically, the angiogenic factor is strongly associated with the inflammatory response during the development of tumors. Additionally, the immunoediting processes are essentially devoted to promoting angiogenesis and modulating the innate and specific immune responses.
This work describes the importance of tumor microenvironment in favouring tumor progression and angiogenesis. Under physiological conditions, angiogenesis is dependent on the balance of positive and negative angiogenic modulators within the vascular microenvironment and requires the functional activities of a number of molecules, including angiogenic factors, extracellular matrix proteins, adhesion molecules and proteolytic enzymes. In normal tissues, vascular quiescence is maintained by the dominant influence of endogenous angiogenesis inhibitors over angiogenic stimuli. Tumor angiogenesis is linked to a switch in the balance between positive and negative regulators, and mainly depends on the release by inflammatory or neoplastic cells of specific growth factors for endothelial cells, that stimulate the growth of the blood vessels of the host or the down-regulation of natural angiogenesis inhibitors. In particular, the inflammatory infiltrate may contribute to tumor angiogenesis, and there are many reports of associations between tumor inflammatory infiltrate, vascularity and prognosis. New therapeutic approaches have been developed with the aim to control tumor angiogenesis through targeting of different components of tumor microenvironment.
The tumor microenvironment has become a very important and hot topic in cancer research within the past few years. The tumor microenvironment is defined as the normal cells, molecules, and blood vessels that surround and feed a tumor cell. As many scientists have realized, studying the tumor microenvironment has become critical to moving the field forward, since there are many players in a tumor’s localized and surrounding area, which can significantly change cancer cell behavior. There is a dual relationship wherein the tumor can change its microenvironment and the microenvironment can affect how a tumor grows and spreads. Tumor Microenvironment in Cancer Progression and Cancer Therapy aims to shed light on the mechanisms, factors, and mediators that are involved in the cancer cell environment. Recent studies have demonstrated that in addition to promoting tumor progression and protecting tumor cells from the spontaneous immune-mediated rejection and different forms of cancer therapeutics, tumor microenvironment can also be a target and mediator of both standard and newly-emerging forms of cancer therapeutics. Thus, the dual role of the tumor microenvironment is the integral focus of the volume. The volume highlights the bi-directional interactions between tumor cells and non-malignant tumor component during tumor progression and treatment. It also focuses on the three groups of the reactive tumor component: stromal cells, blood vessels and the infiltrating immune cells. These three groups are discussed under the lens of their role in promoting tumor growth, shielding the tumor from rejection and from standard forms of cancer therapies. They are emerging as targets and mediators of standard and new forms of potential therapy.
Revealing essential roles of the tumor microenvironment in cancer progression, this book focuses on the role of hematopoietic components of the tumor microenvironment. Further, it teaches readers about the roles of distinct constituents of the tumor microenvironment and how they affect cancer development. Topics include eosinophils, NK cells, γδ T cells, regulatory T Cells, Langerhans cells, hematopoietic stem cells, Mast cells, B cells and Microglia, and more. Taken alongside its companion volumes, Tumor Microenvironment: Hematopoietic Cells – Part B updates us on what we know about various aspects of the tumor microenvironment as well as future directions. This book is essential reading for advanced cell biology and cancer biology students as well as researchers seeking an update on research in the tumor microenvironment.
This edited volume discusses the complexity of tumor microenvironments during cancer development, progression and treatment. Each chapter presents a different mathematical model designed to investigate the interactions between tumor cells and the surrounding stroma and stromal cells. The topics covered in this book include the quantitative image analysis of a tumor microenvironment, the microenvironmental barriers in oxygen and drug delivery to tumors, the development of tumor microenvironmental niches and sanctuaries, intravenous transport of the circulating tumor cells, the role of the tumor microenvironment in chemotherapeutic interventions, the interactions between tumor cells, the extracellular matrix, the interstitial fluid, and the immune and stromal cells. Mathematical models discussed here embrace both continuous and agent-based approaches, as well as mathematical frameworks of solid mechanics, fluid dynamics and optimal control theory. The topics in each chapter will be of interest to a biological community wishing to apply the mathematical methods to interpret their experimental data, and to a biomathematical audience interested in exploring how mathematical models can be used to address complex questions in cancer biology.
One of the current challenges and failures of immunotherapy is in part due to the complex tumor microenvironment (TME) that provides a formidable barrier to immune infiltration and function. The TME consists of various cell types (tumor cells, fibroblasts, endothelial cells, and immune cells), soluble signaling molecules (cytokines, growth factors, and chemokines), and extracellular matrix. On another note, metabolic disturbances in various TME components, such as hypoxia, acidosis, lactate accumulation, and nutrient deprivation, can play a critical role in the tumor progression. Furthermore, genetic and epigenetic dysfunctions are known to be part of the characteristics of cancer development. The immune cells could have a pro- or anti-tumor role in the TME, and their activity might vary in the context of different cancers. Both innate and adaptive immune cells interact with tumor cells through direct contact or through chemokines and cytokines signaling, shaping the tumor's activity and response to therapy.
Revealing essential roles of the tumor microenvironment in cancer progression, this book provides a comprehensive overview of the latest research on the role of interleukins in the tumor microenvironment. Each chapter focuses on the various ways to target the tumor microenvironment by intervention in the interleukin biology, including IL-6, IL-7, IL-10, IL-12, IL-22, IL-23, and IL-24 signaling. Taken alongside its companion volumes, Tumor Microenvironment: The Role of Interleukins – Part B updates us on what we know about various aspects of the tumor microenvironment, as well as future directions. This book is essential reading for advanced cell biology and cancer biology students as well as researchers seeking an update on research in the tumor microenvironment.
This book is focused on the analysis of the role played by immune cell components in the angiogenic process associated with inflammation and tumor growth. Both innate and adaptive immune cells are involved in the mechanisms of endothelial cell proliferation, migration and activation, through the production and release of a large spectrum of pro-angiogenic mediators. These may create the specific microenvironment that favors an increased rate of tissue vascularization. The link between chronic inflammation and tumorigenesis was first proposed by Rudolf Virchow in 1863 after the observation that infiltrating leukocytes are a hallmark of tumors and first established a causative connection between the lymph reticular infiltrate at sites of chronic inflammation and the development of cancer. Tumors were described as wounds that never heal and surgeons have long described the tendency of tumors to recur in healing resection margin and it has been reported that wound healing environment provides an opportunistic matrix for tumor growth. As angiogenesis is the result of a net balance between the activities exerted by positive and negative regulators, this book will also provide information on some anti-angiogenic properties of immune cells that may be utilized for a potential pharmacological use as anti-angiogenic agents in inflammation as well as in cancer. The work is written for researchers in the field and also for graduate students which approach this matter.
Angiogenesis is the physiological process where new blood vessels grow from existing ones, in order to replenish tissues suffering from inadequate blood supply. Perhaps the most studied angiogenic process occurs in solid tumors whose growing mass and expanding cells create a constant demand for additional supply of oxygen and nutrients for survival. However, other physiological and clinical conditions, such as wound healing, ischemic events, autoimmune and age-related diseases also involve angiogenesis. Angiogenesis is a well-structured process that begins when oxygen and nutrients are depleted, leading to the release of chemokines and growth factors that attract immune cells, particularly macrophages and endothelial cells to the site. Macrophages that are recruited to the site, as well as tissue cells and endothelial cells, secrete pro-angiogenic mediators that affect endothelial cells and promote angiogenesis. These mediators include growth factors such as vascular endothelial cell growth factor (VEGF), matrix metalloproteinases (MMPs), as well as low levels of mediators that are usually seen as pro-inflammatory but are pro-angiogenic when secreted in low levels (e.g. nitric oxide (NO) and TNFa). Thus, macrophages play a major role in angiogenesis. Macrophages exhibit high plasticity and are capable of shifting between different activation modes and functions according to their changing microenvironment. Small differences in the composition of activating factors (e.g. TLR ligands such as LPS, anti-inflammatory cytokines, ECM molecules) in the microenvironment may differently activate macrophages to yield classically activated macrophages (or M1 macrophages) that can kill pathogen and tumor cells, alternatively activated macrophages (or M2 macrophages) that secrete antiinflammatory cytokines, resolution macrophages (rM?) that are involved in the resolution of inflammation, or regulatory macrophages (e.g. Myeloid-Derived Suppressor Cells - MDSCs) that control the function of other immune cells. In fact, macrophages may be activated in a spectrum of subsets that may differently contribute to angiogenesis, and in particular non-classically activated macrophages such as tumor-associated macrophages (TAMs) and Tie2-expressing monocytes (TEMs) can secrete high amounts of pro-angiogenic factors (e.g. VEGF, MMPs) or low levels of pro-inflammatory mediators (e.g. NO or TNFa) resulting in pro-angiogenic effects. Although the importance of macrophages as major contributors and regulators of the angiogenic process is well documented, less is known about the interactions between macrophages and other cell types (e.g. tumor cells, normal epithelial cells, endothelial cells) that regulate angiogenesis. We still have only limited understanding which proteins or complexes mediate these interactions and whether they require cell-cell contact (e.g. through integrins) or soluble factors (e.g. the EGF-CSF-1 loop), which signaling pathways are triggered in each of the two corresponding cell types, and how this leads to secretion of pro- or antiangiogenic factors in the microenvironment. The regulation of such interactions and through them of angiogenesis, whether through post-translational modifications of proteins or via the involvement of microRNA, is still unclear. The goal of this Research Topic is to highlight these interactions and their regulation in the context of both physiological and pathological conditions.