Download Free Epithelial Mesenchymal Interactions In Cancer Book in PDF and EPUB Free Download. You can read online Epithelial Mesenchymal Interactions In Cancer and write the review.

gar discusses recent studies of the SF gene promoter that may be relevant to understanding the detailed molecular mechanism(s) by which soluble factors regulate SF production. Polverini and Nickoloff discuss another mechanism by which SF may enhance tumor growth, ie., stimulation of angiogenesis, the formation of new blood vessels from pre-existing microvessels. Angiogenesis is required for continued growth of most solid tumors, and provides a mechanism by which the stroma may continue to grow along with the tumor cells. Although endothelial cells are stromal cells, they express a number of epithelial characteristics including (i) epithelial-like tight junctions and junctional proteins; (ii) the ability to organize into flat­ tened tubular structures; (iii) the c-met receptor protein; and (iv) biologic responsiveness to SF. It is, perhaps, not surprising that vascular endothe­ lial cells may both produce and respond to SF in different situations. 'Epithelialness' may be defined in two ways: (i) expression of generic epithelial structures and proteins (eg., specialized junctions, junctional proteins [eg., cadherins, ZOl], cytokeratins); and (ii) production of specific differentiated products (eg., milk proteins by mammary epithelia, renin by renal tubular epithelia of the juxtaglomerular apparatus). Recent studies suggest that SF Ic-met signalling may mediate epithelia­ mesenchyme interconversion, in part by modifying some of the generic epithelial characteristics. Nusrat discusses the effects of SF on the epithelial junctional apparatus. Relatively little is known about whether and how SF regulates cell-specific differentiation.
This book is a printed edition of the Special Issue "The Epithelial-to-Mesenchymal Transition (EMT) in Cancer" that was published in Cancers
The contribution of epithelia-mesenchyme interaction to normal development (eg., tissue formation) and to neoplasia has become a subject of increasing interest to scientists because of recent progress in deciphering the molecular signals that mediate this interaction. Clearly, some of the same types of molecules (eg., growth factors and their receptors, proteolytic enzymes, cell adhesion molecules, and structural proteins of the extracellular matrix) mediate exchange of information between epithelia and mesenchyme during normal development and malignant growth. However, defects in the regulation of this exchange appear to contribute to malignancy by allowing growth promoting, invasogenic, and angiogenic factors to accumulate within the microenvironment of the tumor. For example, recent studies suggest that abnormal interactions between tumor epithelial cells and stromal mesenchymal cells contribute to the overproduction and accumulation of scatter factor (hepatocyte growth factor), an invasogenic and angiogenic cytokine, in certain types of tumor. The production and and activation of type IV collagenase, a matrix-degrading enzyme required for tumor cell invasion, appears to require intimate cooperation between tumor and stromal cells. The material contained in this volume highlights the state-of-the-art of knowledge of the molecular mechanisms by which epithelia and mesenchyme collaborate, and the abnormalities in these mechanisms that may lead to the development of cancer.
The key aim of the proposed chapter is to provide readers a brief description for the most important parts of the field of circulating tumor cells (CTCs): the core techniques, including negative and positive selection-based CTC isolation, and the differences between them. Most importantly, we will also review the clinical applications and important findings in clinical trials. The evidence-based review will not only help clinicians use CTCs to predict recurrence and foresee the disease-related outcomes but also to inspire the researchers in this field to conduct further investigations.
Epithelial phenotype is a dynamic stage of differentiation that can be modulated during several physiological or pathological events. The rapid conversion to a mesenchymal-like phenotype is called an epithelial-mesenchymal transition (EMT). The Rise and Fall of Epithelial Phenotype is the first book to comprehensively introduce the concept of EMT. The first part of this volume describes main examples and models and explains their physiological relevance. These examples include hydra morphogenesis, gastrulation in mouse, drosophila and sea urchin, as well as neural crest cell migration and heart morphogenesis in vertebrates. Part two reviews in detail, specific EMT molecular pathways covering extracellular induction, transduction and transcription response and modulation of cell-cell adhesion structures. It emphasizes new specific pathways with potential medical applications. EMTs can also be linked to pathological events such as wound healing and cancer progression, as detailed in this section of the book.
Recent studies have highlighted that epithelial-mesenchymal transition (EMT) is not only about cell migration and invasion, but it can also govern many other important elements such as immunosuppression, metabolic reprogramming, senescence-associated secretory phenotype (SASP), stem cell properties, therapy resistance, and tumor microenvironment interactions. With the on-going debate about the requirement of EMT for cancer metastasis, an emerging focus on intermediate states of EMT and its reverse process mesenchymal-epithelial transition (MET) offer new ideas for metastatic requirements and the dynamics of EMT/MET during the entire metastatic cascade. Therefore, we would like to initiate discussions on viewing EMT and its downstream signaling networks as a fulcrum of cellular plasticity, and a facilitator of the adaptive responses of cancer cells to distant organ microenvironments and various therapeutic assaults. We hereby invite scientists who have prominently contributed to this field, and whose valuable insights have led to the appreciation of epithelial-mesenchymal plasticity as a more comprehensive mediator of the adaptive response of cancer cells, with huge implications in metastasis, drug resistance, tumor relapse, and patient survival.
Ultrastructural Pathology
Phenotypic Switching: Implications in Biology and Medicine provides a comprehensive examination of phenotypic switching across biological systems, including underlying mechanisms, evolutionary significance, and its role in biomedical science. Contributions from international leaders discuss conceptual and theoretical aspects of phenotypic plasticity, its influence over biological development, differentiation, biodiversity, and potential applications in cancer therapy, regenerative medicine and stem cell therapy, among other treatments. Chapters discuss fundamental mechanisms of phenotypic switching, including transition states, cell fate decisions, epigenetic factors, stochasticity, protein-based inheritance, specific areas of human development and disease relevance, phenotypic plasticity in melanoma, prostate cancer, breast cancer, non-genetic heterogeneity in cancer, hepatitis C, and more. This book is essential for active researchers, basic and translational scientists, clinicians, postgraduates and students in genetics, human genomics, pathology, bioinformatics, developmental biology, evolutionary biology and adaptive opportunities in yeast. - Thoroughly addresses the conceptual, experimental and translational aspects that underlie phenotypic plasticity - Emphasizes quantitative approaches, nonlinear dynamics, mechanistic insights and key methodologies to advance phenotypic plasticity studies - Features a diverse range of chapter contributions from international leaders in the field
This volume covers classic and modern cell and molecular biology of prostate cancer, as well as novel biomarkers, inflammation, centrosome pathologies, microRNAs, cancer initiation novel biomarkers, inflammation, centrosome pathologies, microRNAs, cancer initiation and genetics, epigenetics, mitochondrial dysfunctions and apoptosis, cancer stem cells, angiogenesis and progression to metastasis, and treatment strategies including clinical trials related to prostate cancer. Cell & Molecular Biology of Prostate Cancer is one of two companion books comprehensively addressing the biology and clinical aspects of prostate cancer. Prostate Cancer: Molecular & Diagnostic Imaging and Treatment Stategies, the companion volume, discusses both classic and the most recent imaging approaches including analysis of needle biopsies, applications of nanoparticle probes and peptide-based radiopharmaceuticals for detection, early diagnosis and treatment of prostate cancer. Taken together, these volumes form one comprehensive and invaluable contribution to the literature.