دانلود کتاب سنجش آنژیوژنز تومور

Growth of solid and hematologic tumors is angiogenesis dependent. Tumor angiogenesis is a well-established hallmark of cancer and is generally viewed as the consequence of an angiogenic switch, that is, a genetic event that endows the tumor with the ability to recruit blood vessels from the neighboring tissue. However, tumors can also grow through alternative mechanisms, including intussusceptive microvascular growth, vascular co-option, and vasculogenic mimicry, which can explain the poor clinical response and resistance to antiangiogenic therapies. In fact, despite the discovery and development of numerous antiangiogenic agents for the treatment of cancer, which have shown promising inhibitory effects in pre-clinical testing, and in some instances tumor regression, these agents have proved very disappointing in clinical trials. Tumor tissue is characterized by rapid proliferation, increased permeability, and disorganized architecture, properties which are a cause or a consequence of inadequate perfusion and oxygenation. The main technical challenge in any study of tumor angiogenesis is the selection of the most appropriate assay. Despite the increasing numbers of both in vitro and in vivo assays, a “gold-standard” angiogenesis assay has yet to be developed; therefore, a combination of assays is required to identify the molecular and /or cellular events in tumor angiogenesis. The inconsistency of data relative to the efficacy of anti-angiogenic treatments highlights the need for rigorous preclinical testing using relevant models and the limitations of each assay being taken into consideration, thus avoiding over interpretation of results. The understanding of these mechanisms is crucial for an effective therapeutic targeting of the angiogenic process. A better insight into the molecular mechanisms and development of methods to induce and observe vessel normalization will result in more potent therapies for cancer. Recent advances in microscopic techniques combined with computational analysis have created new paradigms in studying vascular flow and permeability. The aim of the second edition of this book is to prove a range of methods and protocols for studying tumor angiogenesis in vitro and in vivo to reflect advances in the field. I would like to thank the colleagues who kindly agreed to contribute to this book.