Epithelial Mesenchymal Interactions In Cancer

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.

This book is a printed edition of the Special Issue "The Epithelial-to-Mesenchymal Transition (EMT) in Cancer" that was published in Cancers

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.

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.

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.

The concept of the epithelial-mesenchymal transition (EMT) provides a basis for understanding complex changes in gene expression, molecular function and cell behaviour. This field has undergone explosive growth in the last few years as the concept has spread from developmental biology to the pathologies of cancer and fibrosis. As scientists are on the verge of being able to control or mitigate the process of EMT in some pathological conditions, understanding of its fundamental mechanisms is of vital importance. This special issue brings together selected reviews and new data from the Boden Conference on Epithelial-Mesenchymal Transitions. The reviews highlight developmental, cancer and pathological EMTs, and are rich in detail at the cell and molecular levels. The publication is aimed at cancer biologists, pathologists and developmental biologists who are interested in why cells begin to move, and the genes and molecules involved in this process.