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This book represents the first compilation of the major research findings regarding Maspin a mammary serpin (or serine) protease inhibitor. Maspin was originally discovered through subtractive hybridization and differential display analyses, comparing the differences in gene expression in normal mammary epithelium and invasive carcinoma cells. This work originated in the laboratory of Dr. Ruth Sager, a world-renowned geneticist, at the Dana Farber Cancer Institute and Harvard Medical School. The first introduction of Maspin to the research community occurred as a report in Science (v263:526-529, 1994), and described the unique tumor-suppressing activity of this novel gene in human mammary epithelial cells.
This book provides a broad and rich outline of the epigenetic mechanisms involved in cancer progression and the generation of metastasis. It describes the tumor suppressor genes undergoing transcriptional silencing by CpG island promoter hypermethylation in the different tumor types of the human anatomy and their association with tumoral behaviour. It also provides a comprehensive insightful look at the molecular players involved in DNA methylation, histone modification and chromatin remodelling complexes causing epigenetic lesions linked to the metastasic phenotypes. Finally, it explains how epigenetic lesions associated with cancer spreading can be targeted using new and potent chemotherapy drugs. The book is a state-of-the-art reference to all scientific researchers and clinicians interested in the understanding of the biological processes leading to tumor dissemination and to those that are keen to translate this knowledge to a better management of cancer patients. Each contributor is a specialist in their epigenetic area and their joint effort has created a unique view of the DNA methylation, histone and chromatin changes that define cancer metastasis.
The spread of cancer cells from their organ of origin to distant tissues is called metastasis. Cancer metastasis is the main cause of death from cancer, and in many cases is difficult to detect or treat. The process by which tumour cells become metastatic is complex and involves many stages, including detachment of cells from the main tumour mass, degradation of the surrounding extra-cellular matrix, invasion into nearby blood vessels, travel and survival through the circulatory system, attachment to a vessel wall, extra-vasation, degradation of the extra-cellular matrix into a distant tissue/organ, and the development of a novel blood supply. In order to accomplish this process, the cells acquire characteristics which are important for each stage. Recently, a class of genes known as metastasis suppressors' has been the subject of intense investigation. For some metastasis suppressor genes, there is strong evidence from both in vitro and in vivo studies to demonstrate key roles in the metastatic process, for others data is much more limited, and their importance uncertain. In this book, chapters are devoted to providing up-to-date summaries of our understanding of individual metastasis suppressor genes. Each is written by a leading authority in the study of that gene. Topics covered include discussions on how each metastasis suppressor was discovered, the mechanisms underlying their loss of expression in tumours and tumour cell lines, their proposed molecular functions, and the consequences to a tumour cell of the loss of this function. This compilation aims to provide, in a single volume, comprehensive information that will be valuable to all scientists working in cancer research, to students needing to understand molecular events that regulate tumour progression and the acquisition of metastasis, and to clinicians who might wish to know more of the roles of potentially new markers for cancer diagnosis and prognosis.
Serpins constitute a superfamily of proteins that possess a unique tertiary structure and mechanism of proteinase inhibition. In humans, serpins constitute 10% of the plasma proteins and are best known as critical regulators of both the thrombotic and fibrinolytic systems. Serpins also participate in the regulation of the complement cascade, angiogenesis, tumor metastasis, apoptosis and innate immunity. Considering the importance of these molecules in regulating proteolytic cascades, it is not surprising to find that loss- and gain-of-function mutations result in significant human diseases.Massive thrombosis or bleeding, hereditary angioedema, Alzheimer's disease, diabetic angiopathy and tumor invasion are some of the human diseases associated with serpins. In addition, mutations that alter serpin conformations (the serpinopathies) lead to lung disease, cirrhosis and a form of familial dementia. The goal of this text is to present the current knowledge on the molecular and cellular basis of serpins and their diseases.
Serpins are a group of proteins with similar structures that were first identified as a set of proteins able to inhibit proteases. The acronym serpin was originally coined because many serpins inhibit chymotrypsin-like serine proteases. This volume of Methods in Ezymology is split into 2 parts and comprehensively covers the subject.
The book provides an comprehensive overview on biology, genetics and cellular functions of serpins (serine protease inhibitors) in health and disease. With over 1000 members serpins are the most diverse family of protease inhibitors. Latest groundbreaking research findings are presented and broaden the understanding on inhibitory and non-inhibitory serpins, not only in mammalian organisms but also in insects, worms, plants and viruses.​
Genetically-engineered mouse models for cancer research have become invaluable tools for studying cancer biology and evaluating novel therapeutic approaches. This volume focuses on state-of-the-art methods for generating, analyzing and validating such models for studying aspects of human cancer biology. Additionally, these models are emerging as important pre-clinical systems in which to test cancer prevention and therapeutic strategies in order to select compounds for testing in clinical trials.
Proceedings of an International Symposium held in Chapel Hill, North Carolina, April 13-16, 1996
This volume highlights the expression of specific adhesion molecules within human cancer tissues. It details the expression signatures from published DNA microarray and immunohistochemistry studies. Coverage discusses the concept that the alteration of specific adhesion molecules influence the cancer migration ability and cancer damage responses, both features are essential for the survival of an invading tumor cell.
Prostate cancer is diagnosed commonly in the course of general health screening. Very often it is difficult to tell whether the cancer will be aggressive and lethal or will be so slow growing that it will not affect the patient's survival. Treatment can have a major impact on the patient's health-related quality of life. This book presents cutting-edge research in predicting the behavior of localized and metastatic cancer, targeted treatment of cancer that has spread minimally, response to newer methods of treatment, and rehabilitation of patients.