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Author: Gaspar Banfalvi Publisher: Springer Science & Business Media ISBN: 9400773358 Category : Medical Languages : en Pages : 290
Book Description
Homeostasis. The health of an organism is influenced by external and internal changes that may lead to the loss of homeostasis. Under healthy conditions organisms compensate these changes. If compensation fails disease ensues. Attention will be paid to lifestyle, environmental changes, genetic makeup and health system. It will be answered how lifestyle, environment, genetic makeup and social conditions help to maintain or upset the biological balance and lead to cancer. Tumor formation. To understand this process the transfer of intracellular and the pathways of extracellular information (signal transduction) will be reviewed briefly. Loss of cellular balance may lead to cell death (.e.g. apoptosis) or to rapid cell growth of cells leading to tumor formation. Metastasis. Animal tumor models serve to understand the spread of the primary tumor cells to distant locations of the organism. Different types of tumors and metastases will be reviewed.
Author: Gaspar Banfalvi Publisher: Springer Science & Business Media ISBN: 9400773358 Category : Medical Languages : en Pages : 290
Book Description
Homeostasis. The health of an organism is influenced by external and internal changes that may lead to the loss of homeostasis. Under healthy conditions organisms compensate these changes. If compensation fails disease ensues. Attention will be paid to lifestyle, environmental changes, genetic makeup and health system. It will be answered how lifestyle, environment, genetic makeup and social conditions help to maintain or upset the biological balance and lead to cancer. Tumor formation. To understand this process the transfer of intracellular and the pathways of extracellular information (signal transduction) will be reviewed briefly. Loss of cellular balance may lead to cell death (.e.g. apoptosis) or to rapid cell growth of cells leading to tumor formation. Metastasis. Animal tumor models serve to understand the spread of the primary tumor cells to distant locations of the organism. Different types of tumors and metastases will be reviewed.
Author: Wei-Lin Jin Publisher: Frontiers Media SA ISBN: 2832528201 Category : Science Languages : en Pages : 279
Book Description
Systemic homeostatic mechanisms include several aspects, such as metabolic, neuroendocrine, immune, and physiological homeostasis. Irreversible damage or reversible imbalance of such homeostatic processes may initiate cancers by altering the regulation of the molecular machinery. Systemic homeostasis-related genes have been found to be intimately involved in oncological processes and in some instances have shown prognostic value. Thus, future gene targeting approaches for cancer should not only focus on classical cancer drivers but also address systemic homeostasis-related genetic mechanisms. Identification of systemic homeostasis-related genes with diagnostic, prognostic or therapeutic value can advance translational cancer research. Increasing numbers of research studies have reported systemic homeostasis-related genes’ relevance to various types of cancer. For example, cancer cells have been shown to activate a critical mechanism of oxygen homeostasis—hypoxia inducible factors (HIFs) family genes, in order to adapt to the tumor microenvironment and develop into a more aggressive phenotype. In addition, methylene tetrahydrofolate dehydrogenase (MTHFD) family genes are involved in mitochondrial one-carbon metabolism, which is essential for maintaining systemic metabolic homeostasis, and have recently been found overexpressed in many cancers and have been correlated to poor survival outcomes. The overexpression of transferrin family genes with iron transporting function has been linked with iron accumulation, which is a known initiating factor in cancer. Another example is Forkhead box O (FOXO) family genes, which serve as a critical regulator of immune homeostasis and can regulate cancer immunity by negatively regulating the expression of immunosuppressive gene-programmed death 1 ligand 1 (PD-L1).Apart from these examples, other systemic homeostatic mechanisms such as glucose homeostasis, energy homeostasis, lipid homeostasis, phosphate homeostasis, cholesterol homeostasis, and mineral homeostasis may also be implicated in cancer pathogenesis. Although accruing research is focused on describing systemic homeostatic mechanisms in cancer biology, several research questions remain unaddressed. The utilization of recent analytic tools and bioinformatics as systems biology approaches has the potential to address these research gaps. Therefore, in this special issue we will collect articles focusing on the application of bioinformatics and systems biology based investigations of systemic homeostatic mechanisms in malignant diseases. Both original research and review articles are welcomed, however publications based on the analysis on only one database will not be accepted (e.g. TCGA).
Author: Yoshiro Maru Publisher: Springer Nature ISBN: 9811617570 Category : Medical Languages : en Pages : 531
Book Description
This book, now in a thoroughly revised and updated second edition, provides the latest information on cancer metastasis from the perspective of inflammation and presents new ideas on the complicated mechanisms of metastasis and potential therapeutic targets. Key features include discussion of mechanisms recently identified to be involved in the resolution phase of inflammation, presentation of the latest evidence regarding the roles of endogenous TLR4 ligands in metastasis, and thorough explanation of the concept of homeostatic inflammation and current understanding of the significance of its dysregulation for metastasis. Structure-based thinking is another important element of the book, and it is proposed that inflammation forms a functional triangle with angiogenesis and coagulation, at the center of which cancer is located. Examples of the many additional specific topics covered in this edition include the functional involvement of new types of RNA in cancer, the insights offered by recent advances in bioinformatics, and the potential of a casein kinase 1α inhibitor in the treatment of acute myeloid leukemia. The book will be a valuable update and resource for both experienced and younger researchers. Homeostasis, originated from an idea of internal milieu by Claude Bernard, is eventually maintained by endogenous elements. The essential features of inflammation are leukocyte mobilization and increased vascular permeability, which could take place in many homeostatic or physiological conditions at low levels. Homeostatic inflammation is a concept to explain pathological settings such as metastasis in which irrespective of its level those inflammatory features are misused with endogenous molecules (see Chap. 14,15). As inflammation comprises many biological fields, targeting a single molecule for a disease could potentially make a therapeutic contribution to other diseases. For example, one focus is applied here to the roles of calprotectin in lung metastasis, which is implicated in psychiatric disorders and COVID-19 as shown by recent evidence.
Author: Sam Thiagalingam Publisher: Cambridge University Press ISBN: 0521493390 Category : Mathematics Languages : en Pages : 597
Book Description
An overview of the current systems biology-based knowledge and the experimental approaches for deciphering the biological basis of cancer.
Author: Charles Swanton Publisher: Perspectives Cshl ISBN: 9781621821434 Category : Medical Languages : en Pages : 350
Book Description
Tumor progression is driven by mutations that confer growth advantages to different subpopulations of cancer cells. As a tumor grows, these subpopulations expand, accumulate new mutations, and are subjected to selective pressures from the environment, including anticancer interventions. This process, termed clonal evolution, can lead to the emergence of therapy-resistant tumors and poses a major challenge for cancer eradication efforts. Written and edited by experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine examines cancer progression as an evolutionary process and explores how this way of looking at cancer may lead to more effective strategies for managing and treating it. The contributors review efforts to characterize the subclonal architecture and dynamics of tumors, understand the roles of chromosomal instability, driver mutations, and mutation order, and determine how cancer cells respond to selective pressures imposed by anticancer agents, immune cells, and other components of the tumor microenvironment. They compare cancer evolution to organismal evolution and describe how ecological theories and mathematical models are being used to understand the complex dynamics between a tumor and its microenvironment during cancer progression. The authors also discuss improved methods to monitor tumor evolution (e.g., liquid biopsies) and the development of more effective strategies for managing and treating cancers (e.g., immunotherapies). This volume will therefore serve as a vital reference for all cancer biologists as well as anyone seeking to improve clinical outcomes for patients with cancer.
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: Keshav Singh Publisher: Springer Science & Business Media ISBN: 0387848355 Category : Medical Languages : en Pages : 294
Book Description
Nearly a century of scientific research has revealed that mitochondrial dysfunction is one of the most common and consistent phenotypes of cancer cells. A number of notable differences in the mitochondria of normal and cancer cells have been described. These include differences in mitochondrial metabolic activity, molecular composition of mitochondria and mtDNA sequence, as well as in alteration of nuclear genes encoding mitochondrial proteins. This book, Mitochondria and Cancer, edited by Keshav K. Singh and Leslie C. Costello, presents thorough analyses of mitochondrial dysfunction as one of the hallmarks of cancer, discusses the clinical implications of mitochondrial defects in cancer, and as unique cellular targets for novel and selective anti-cancer therapy.
Author: Hangwen Li Publisher: ISBN: Category : Languages : en Pages : 312
Book Description
The recently resurrected cancer stem cell (CSC) theory sheds new light on understanding tumor biology. Most solid tumors have now been shown to contain CSCs, i.e., stem cell-like cancer cells. These cells, although generally rare, appear to be highly tumorigenic and may be the cells that drive tumor formation, maintain tumor homeostasis, and mediate tumor metastasis. In order to test whether any given human tumor cell population has CSC properties, the relatively enriched single tumor cells have to be put into a foreign microenvironment in a recipient animal to test their tumorigenic potential. Furthermore, various in vitro assays can be performed to demonstrate that the presumed CSCs have certain biological properties normally associated with the stem cells (SCs). Herein, I first present a comprehensive review of the experimental methodologies that our lab has been using in assaying putative prostate cancer (PCa) SCs in culture, xenograft tumors, and primary tumor samples. Clonal morphology is one of the critical properties of cultured cancer cells that has been largely ignored. Interestingly, long term-cultured human epithelial cancer cells form holoclones, meroclones, and paraclones, and tumor cell holoclones have been hypothesized to harbor stem-like cells. Using PC3 human prostate carcinoma cells as a model, we provide direct experimental evidence that tumor cell holoclones contain stem-like cells that can initiate serially transplantable tumors. Importantly, holoclones derived from either cultured PC3 cells or holoclone-initiated tumors can be serially passaged and regenerate all three types of clones. In contrast, meroclones and paraclones cannot be continuously propagated and fail to initiate tumor development. Phenotypic characterizations reveal high levels of CD44, [alpha]2[beta]1 integrin, and [beta]-catenin expression in holoclones, whereas meroclones and paraclones show markedly reduced expression of these markers. These observations have important implications in understanding morphologic heterogeneities and tumorigenic hierarchies in human epithelial cancer cells. PCa metastasis represents the worst outcome, and, if unchecked, will eventually kill the patient. Although many PCa cell-intrinsic molecules and end-organ factors have been implicated in the metastatic dissemination of PCa cells, the role of primary tumor microenvironment and the nature of the metastatic PCa cells remain poorly defined. By establishing a reliable and quantifiable experimental PCa metastasis model in NOD/SCID mice, we show that PCa cells implanted orthotopically (i.e., in the prostate) metastasize much more extensively and widely than those implanted ectopically (i.e., subcutaneously or s.c). Microarray-based gene expression profiling reveals that the orthotopically implanted human PCa cells prominently overexpress not only several classes of molecules involved in proteolysis/invasion/angiogenesis and inflammation, but also numerous developmental and SC regulating genes. These latter observations suggest that the orthotopic microenvironment (i.e. mouse prostate) appears to be promoting the manifestation of CSC phenotypes and these CSCs might be involved in enhanced metastasis in the orthotopic microenvironment and later distant organ metastasis. In support, shRNA-mediated knockdown in many metastatic and CSC genes greatly inhibits PCa cell metastasis. Importantly, PCa cells that express high levels of osteopontin (OPN) or CD24, when prospectively purified out and used in spontaneous metastasis assays, demonstrate high metastatic capacities characteristic of metastatic CSCs. In sharp contrast, PCa cells negative for OPN and CD24 expression show little metastatic property. Finally, we provide multiple pieces of additional evidence that metastatic/metastasizing PCa cells possess CSC properties.
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: Gaspar Banfalvi
Author: Gaspar Banfalvi
Author: Wei-Lin Jin
Author: Yoshiro Maru
Author: Sam Thiagalingam
Author: Zhijie Xu
Author: Charles Swanton
Author: Maryse Dagenais
Author: Keshav Singh
Author: Hangwen Li
Author: Bharat B. Aggarwal